Al-Najam Journal of Medical and Life Sciences
Al-Najam Journal of Medical and Life Sciences (ANJMLS) is an international, peer-reviewed, open-access journal committed to advancing research across medical, clinical, and life sciences disciplines. The journal serves as a scholarly platform for researchers, clinicians, and academicians to disseminate high-quality scientific work that contributes to improved healthcare and biological understanding. ANJMLS accepts original research articles, systematic reviews, meta-analyses, case reports and short communications in basic sciences, translational sciences, and applied sciences. It covers biomedical research, public health, clinical medicine, laboratory sciences, biotechnology, and the new innovations in the life sciences. The journal promotes interdisciplinary research that facilitates laboratory findings to clinical and community action. ANJMLS follows strict editorial standards and ethical publication ethics as well as open-minded peer-review procedures. There is a special focus on evidence-based studies that can resolve regional and global issues related to health. The journal helps to ease the early-career researchers through facilitating scientific integrity, reporting clarity, and excellence of methods. ANJMLS is helping to make scholarly contributions more visible and more widely impactful globally by making them timely published and widely available. ANJMLS strives to promote scientific development and promote health outcomes of various populations through knowledge sharing and academic interaction.
Al-Najam Journal of Medical and Life Sciences (ANJMLS) follows the Attribution Creative Commons-Non commercial (CC BY-NC) license which allows the users to copy and redistribute the material in any medium or format, remix, transform and build upon the material. The users must give credit to the source and indicate, provide a link to the license, and indicate if changes were made. However, the CC BY-NC license restricts the use of material for commercial purposes (Further details are available at website. The Editorial Board of the ANJMLS endeavors to ensure the accuracy, integrity, and quality of all published content. However, the responsibility of opinions, interpretations, and conclusions expressed in the published articles rests entirely with the authors and do not necessarily reflect the views of the Editorial Board, publisher, or affiliated institutions.
Patterns of Post-COVID Symptoms Among Recovered Patients Attending Follow-Up Clinics, A cross-sectional analysis
Background: Post-COVID syndrome is a serious public health problem that is caused by persisting symptoms after the acute phase of SARS-CoV-2 infection. The study aimed to evaluate the symptom pattern of recovered patients in follow-up clinics and to classify factors related with the burden of symptoms. Methods: A cross-sectional study (n=150) used non-probability technique to gather data on socio-demographic characteristics, clinical history during persistent symptoms of COVID and acute COVID infection. SPSS version 26.0, data analysis was carried out. Descriptive statistics, chi-squared tests, multiple regression analysis and Pearson's correlation were performed to identify associations between variables (p-value < 0.05). Results: COPD symptoms were present in 71.3% of patients and the most repeated symptoms were fatigue (54.7%), dyspnea (42.7%) and sleep disturbance (38.7%). Patients with severe acute infection, ICU admission, hospitalization, oxygen therapy and significantly had more symptoms burden (p < 0.001). The acute disease severity positively and significantly correlated with number of post-COVID symptoms (r = 0.41, p<0.001). Severe acute infection (β = 0.36, p < 0.001), intensive care unit (ICU) admission (β = 0.29, p = 0.002), and oxygen therapy (β = 0.24, p = 0.006) were found to be significant factors in predicting a higher symptom burden. The model explained 52% of the variance in the post-COVID symptom burden (R² = 0.52). Conclusions: COVID-19 patients who have recovered are still suffering from symptoms, such as fatigue and respiratory issues. Acute infection severity is a good predictor of long-term symptom burden.
Copyright (c) 2026 Attiya Khizar, Shahida Anjum, Momina Rehmat (Author) https://creativecommons.org/licenses/by-nc/4.0/
Utilizing the summary of Diabetes self care activities scale to predict Metabolic outcomes Body Mass Index and Therapeutic dependencies
Background: Diabetes mellitus is a chronic metabolic disease which needs to be self-managed continuously to maintain optimal glycemic control and to avoid complications. The study aimed to evaluate self-care activities of people with diabetes and their association with glycemic control. Methods: This cross-sectional study (n=100) collected data using the structured questionnaires and Summary of Diabetes Self-Care Activities (SDSCA) scale. Medical records were used to collect clinical data, such as fasting blood glucose, glycated hemoglobin (HbA1c), body mass index (BMI), diabetes duration and treatment modalities. The statistical analysis was carried out in SPSS version 26.0 with p-value< 0.05. Results: The mean self-care score was 53.8 ± 11.4, while the mean HbA1c level was 8.1 ± 1.5%. The mean HbA1c level was statistically significant in different categories of self-care (F = 21.84, p < 0.001) with a decreasing trend from poor to good self-care. Self-care scores showed significant negative correlations with HbA1c (r = −0.68, p < 0.001), fasting blood glucose (r = −0.59, p < 0.001), BMI (r = −0.31, p = 0.002), and duration of diabetes (r = −0.25, p = 0.012). Multiple linear regression analysis identified self-care score (β = −0.49, p < 0.001), BMI (β = 0.22, p = 0.015), diabetes duration (β = 0.18, p = 0.031), and insulin therapy (β = −0.16, p = 0.048) as significant predictors of HbA1c. Conclusions: Diabetic patients' self-care is heavily correlated with glycemic outcomes. Low HbA1c levels and good blood sugar control were associated with better self-care behaviors.
Copyright (c) 2026 Aliya Ramazan, Saira Habib, Maryum (Author) https://creativecommons.org/licenses/by-nc/4.0/
Life Beyond the Clinic: Quantifying the Negative Correlation Between Treatment Duration and Survivor Quality of Life in Breast Cancer Patients
Background: Improvements in early diagnosis and treatment have led to significant improvements in breast cancer survival, but long-term survivors may still have reduced quality of life (QoL) affected by physical, psychological and social aspects. The purpose of this study was to explore the quality of life of breast cancer survivors and to evaluate the correlation between treatment duration and quality of life. Methods: This cross sectional study with 120 breast cancer survivors used non-probability consecutive sampling technique with a Structured questionnaire to assess quality of life were used to gather data on physical, emotional, social and functional domains. Descriptive data analysis was performed, and inferential data analysis was done through one-way ANOVA, Pearson correlation, independent t-test, and multiple linear regression (SPSS 20.0, P value <0.05). Results: The average total QoL score was 62.4 ± 13.7. Patients with a shorter treatment duration (<1 year) had significantly higher scores (71.2 ± 10.5) than patients with a longer treatment duration (>3 years) (55.1 ± 12.3), (p < 0.001). Significant negative correlations were observed between treatment duration and overall QoL (r = −0.56, p < 0.001), physical well-being (r = −0.49, p < 0.001), and emotional well-being (r = −0.52, p < 0.001). Multiple linear regression showed that treatment duration (p < 0.001, β = −0.44), cancer stage (p = 0.002, β = −0.23) and chemotherapy exposure (p = 0.044, β = −0.19) were significant factors in the reduction of QoL. The model elucidated 48% of the variance in QoL outcomes (R² = 0.48, p < 0.001). Conclusions: The length of treatment is a significant factor in quality of life among the survivors of breast cancer and is correlated with poor quality of life. New targeted survivorship care programs emphasizing lifelong follow-up, psychological support, and physical rehabilitation are needed to enhance the well-being of this patient population.
Copyright (c) 2026 Rimsha Ali, Maham Khizar, Maryum Ehsan (Author) https://creativecommons.org/licenses/by-nc/4.0/
Quantifying Fatigue in Chronic Kidney Disease: Its Correlation with Disease Severity and Biochemical Parameters
Background: Chronic Kidney Disease is a chronic health condition with physical and psychological impacts. This study determined the level of fatigue in patients with CKD and its association with the severity of the disease and some clinical parameters. Methods: A cross-sectional study was designed and performed on 80 patients with CKD who were attending the nephrology clinics and dialysis units. Structured questionnaires and a review of medical records were used to gather demographic and clinical information. Fatigue Severity Scale (FSS) was used for assessing fatigue. The clinical parameters such as estimated glomerular filtration rate (eGFR), serum creatinine, haemoglobin level, and duration of CKD were noted. The descriptive and inferential statistics were applied via SPSS version 26.0. Results: Participants had moderate to high fatigue reflected in a mean fatigue severity score of 42.8 ± 10.5. 47.5% of patients reported moderate fatigue and 35.0% severe fatigue. There was a significant increase in fatigue severity from the CKD 2 stage (31.4 ± 7.2) to the CKD 5 stage (53.3 ± 7.6) (p < 0.001). Significant positive correlations were observed between fatigue and age (r = 0.31, p = 0.005), disease duration (r = 0.38, p < 0.001), and serum creatinine levels (r = 0.59, p < 0.001). Significant negative correlations were found between fatigue and haemoglobin (r = −0.54, p < 0.001) as well as eGFR (r = −0.62, p < 0.001). Reduced eGFR (β = −0.41, p < 0.001), low haemoglobin (β = −0.33, p = 0.002) and high serum creatinine (β = 0.29, p = 0.006) were significant factors associated with fatigue severity in multiple regression analysis. Conclusions: Fatigue is a very common symptom in patients with chronic kidney disease, and gets worse as the disease advances. Fatigue severity was linked to decreased kidney function and anemia.
Copyright (c) 2026 Mohsin Ali, Asif Rehman, Mahnoor Khan (Author) https://creativecommons.org/licenses/by-nc/4.0/
Copyright (c) 2026 ANJMLS https://creativecommons.org/licenses/by-nc/4.0/
Knowledge of Medication Management and Therapeutic Care Practices Among Nurses Caring for Older Adults: A Cross-Sectional Study
Background: Older people often have several chronic diseases, and they need to take multiple medications and undergo ongoing therapy. The purposes of this study were to determine the knowledge of medication management and therapeutic care practices among caregivers (nurses) of older adults and to explore factors associated with the level of knowledge. Methods: A cross-sectional study design (n=120) via convenience sampling technique used a structured self-administered questionnaire to evaluate knowledge about medication administration, drug interactions, adverse drug reactions, managing polypharmacy, therapeutic monitoring and educating patients. Data were analyzed using SPSS version 26.0 with p-value < 0.05 as statistically significant. Results: The overall mean score of their knowledge was 78.4 ± 10.6 out of 100. It was observed that the majority of the nurses (61.7%) had good knowledge, 28.3 % had moderate knowledge, and 10.0% had poor knowledge. A significant correlation was found between knowledge and some factors, such as higher scores with increasing clinical experience and higher scores with those who had recently completed professional training (p< 0.05). There were positive relationships between knowledge and years of experience (r = 0.49, p < 0.001) as well as between knowledge and attendance in continuing education activities (r = 0.52, p < 0.001). Multiple regression analysis showed that continuing professional education (β = 0.38, p < 0.001) and clinical experience (β = 0.31, p = 0.002) were significant factors related to knowledge about medication management and therapeutic care practices. Conclusion: The majority of nurses showed evidence of good knowledge of medication management and therapeutic practices for older people. There was a significant contribution to higher knowledge level from professional training and clinical experience.
Copyright (c) 2026 Naila Anjum, Sadia Mukarram, Nimra Rehman (Author) https://creativecommons.org/licenses/by-nc/4.0/
Assessment of Cognitive Function Using the Mini-Mental State Examination Among Community-Dwelling Older Adults: A Cross-Sectional Study
Background: Cognitive decline is a common concern of the elderly, which can have a negative impact on memory, function, independence and quality of life for older individuals. The purpose of this study was to evaluate cognitive functioning in older people in the community using the MMSE and to determine the demographic and health-related factors that are associated with cognitive functioning. Methodology: Cross sectional survey based (n=120) structured questionnaire included demographic data, housing status, and chronic medical conditions (i.e. diabetes, hypertension, asthma, epilepsy, lung disease, heart disease, cancer, HIV, AIDS). The cognitive status was assessed by MMSE. Descriptive analysis, independent-samples t-tests, Pearson correlation analysis and multiple linear regression were used to analyze the data obtained (p-value < 0.05). Results: The average total MMSE score was 24.9 ± 3.8. Of all participants, 59.2% had normal cognitive function; 32.5% had MCI and 8.3% had MCI (moderate). The age groups and educational levels/housing status differed significantly from each other in MMSE score (p < 0.05). Correlation between age and MMSE score was strong and negative (r = −0.61, p < 0.001) while educational level was strongly and positively correlated with MMSE (r = 0.58, p < 0.001). Educational level was the most significant positive predictor (β = 0.37, p < 0.001) while age was the most significant negative predictor (β = −0.42, p < 0.001) in multiple linear regression. Conclusion: The cognitive function was normal in the majority of older adults living in the community, but a significant portion of study participants had mild to moderate impairment. Better cognitive outcomes were correlated with education and older age was correlated with poorer cognitive performance.
Copyright (c) 2026 Komal Zara, Adeela Shafique, Nimra Rehman (Author) https://creativecommons.org/licenses/by-nc/4.0/
Assessment of Laboratory Knowledge, Practical Competency, and Learning Outcomes Among Undergraduate Medical Students
Background: Medical education is based on the support of theory, academic activity and competency in the laboratory. The aim of this study was to assess the academic engagement, lab exposure and knowledge scores of medical undergraduate students and to statistically associate them. Methods: This cross sectional analytical study (n=120) used stratified sampling technique and a structured questionnaire was developed specifically for the study, which included a knowledge assessment score test (15 items) to assess the level of knowledge, a frequency score test to assess the level of academic engagement (study hours, attendance and use of digital learning), a hands-on participation score test to assess the level of exposure on the laboratory, and a supervision score test to assess the level of supervision in the laboratory. SPSS v26 was used for the statistical analysis. Descriptive statistics (mean ± SD and percentages) were calculated. Independent t-test and one-way ANOVA were used for group comparisons. Pearson correlation coefficient and Chi square test were used to examine the relationship between the variables, at p < 0.05 significance level. Results: Out of 120 participants, the mean age was 21.1 ± 1.6 years with 52.5% of females. There was a significant difference in the knowledge scores between students with high and low laboratory exposure (68.9 ± 9.8 vs 54.2 ± 10.5, p < 0.001). There was a moderate positive correlation between the study hours and knowledge score (r = 0.41, p < 0.01). Academic engagement (ANOVA, F = 6.72, p = 0.002) was a significant factor for laboratory competency scores. A significant correlation between year of study and level of lab participation was found using a chi-square test (χ² = 14.3, p = 0.01). Generally, regression analysis showed that laboratory exposure had the highest beta (0.36, p < 0.001) that contributed to the knowledge score. Conclusions: Academic involvement and practical experience in the laboratory have a significant effect on the knowledge building and skill acquisition of medical students.
Copyright (c) 2026 Tanzeel Qadri, Saba Ikram, Mohsin Khalil (Author) https://creativecommons.org/licenses/by-nc/4.0/
Region-Specific Alterations in Brain UPE in Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common cause of dementia in the world, and it is marked by deterioration of cognitive functions; the formation of amyloid-β in the brain; and tau, the formation of tau pathology; synaptic degeneration; and local susceptibility, especially in the hippocampus and association cortices. The most common processes identified to cause neuronal injury and disease development are oxidative stress and mitochondrial dysfunction. Ultraweak photon emission (UPE), a spontaneous biophotonic emission in response to oxidative metabolic reactions, has become a possible cellular redox imbalance and neural activity indicator. Since oxidative changes in AD are region-specific, UPE can indicate region-specific neurodegeneration. Nevertheless, existing research on brain UPE in AD is insufficient and primarily focuses on global oxidative indicators, rather than regional patterns. Lack of systematic analysis of the region-specific UPE changes is also a major gap in research. This aims the regional differences in brain UPE in Alzheimer’s, and determine whether they correlate with oxidative imbalance and neuropathological severity. The detection of specific UPE signatures could contribute to the enhanced comprehension of spatial disease heterogeneity and aid in its advancement as a possible functional biomarker of the early disease detection and progression tracking.
Copyright (c) 2026 Hamayun Saqib (Author) https://creativecommons.org/licenses/by-nc/4.0/
Cytokine-Mediated Intestinal and Systemic Immune Dysregulation in Inflammatory Bowel Disease, Celiac Disease, and Autoimmune Hepatitis: A Systematic Review and Meta-Analysis of Biomolecular Mechanisms and Therapies
Background: Cytokine-mediated immune dysregulation is important in the pathogenesis of autoimmune and inflammatory diseases, such as inflammatory bowel disease, celiac disease, and autoimmune hepatitis. This paper set out to undertake a systematic review of cytokine-mediated immune mechanisms, especially the IL-17, in these conditions. Methods: PRISMA 2020 was used in this systematic review. Up to March 2026, the electronic databases such as PubMed, Scopus, Web of Science, and Google Scholar were searched. Articles that reported cytokine levels or immune biomarkers in patients with inflammatory bowel disease, celiac disease, or autoimmune hepatitis versus those without any disease or animal studies, reviews, case reports, and studies of which quantitative cytokine levels were not measured were excluded. The synthesis of data was done qualitatively and quantitatively and meta-analysis was done on the synthesized data using random-effects model to estimate pooled standardized mean differences. Results: 443 articles were found, out of which 15 articles were eligible to include in the systematic review, and a subset of them was added to the meta-analysis. The combined findings showed very high levels of circulating IL-17 in celiac disease patients in comparison with healthy controls, but no significant differences were found between Crohn disease patients and autoimmune hepatitis patients. In a number of the observational studies, the risk of bias was moderate and was assessed. Conclusion: IL-17–mediated immune dysregulation is significantly elevated in celiac disease but not consistently in Crohn’s disease or autoimmune hepatitis, while IL-23 significantly increased in autoimmune hepatitis. These findings highlight disease-specific roles of IL-23/Th17-related pathways and the need for larger, standardized studies.
Copyright (c) 2026 Asmat Ullah Khan, Hina Murtaza, Raheela Khawar (Author) https://creativecommons.org/licenses/by-nc/4.0/
Prevalence and Concentration of Microplastics in Human Biological Matrices: A Systematic Review and Meta-Analysis
Background: Microplastics are ubiquitous environmental contaminants, which have been detected in many human biological matrices, but information on the presence, concentration and polymer types of microplastics in different matrices is fragmented. This systematic review and meta-analysis aimed to pool data on the detection rates, particle-based concentrations, and relative abundances of polypropylene (PP) and polyethylene (PE) in human biological samples. Methods: The study followed PRISMA 2020 guidelines. PubMed, Scopus, Web of Science, and Google Scholar were searched between January 2021 and April 2026. Original research publications that reported quantitative detection rates, mean concentrations, or polymer proportions in human tissues or fluids were considered. The risk of bias was assessed using the modified NOS, JBI, and ROBINS-I tool, and the certainty of evidence was graded using the GRADE approach. Meta-analysis was conducted using the Revman Tool. Results: Fifteen studies satisfied the inclusion criteria. Nine studies contributed to the detection rate meta-analysis (343 persons), providing a pooled prevalence of 0.91 (95% CI: 0.78-0.98), with significant heterogeneity (I²=87%). Seven studies (133 samples) reported particle-based concentration data, with a pooled mean of 16.0 particles/g (95% CI: 8.3-23.6; I² = 92%). The polymer proportions showed considerable heterogeneity (I²≥87%), with individual-based proportions of 0.49 (95% CI: 0.28-0.70) for PP and 0.48 (95% CI: 0.19-0.78) for PE, and particle-based proportions of 0.23 (95% CI: 0.10-0.43) for PP and 0.15 (95% CI: 0.05-0.36) for PE. Conclusion: Microplastics were found in the majority of human biological samples, albeit in varying amounts; the most often discovered polymers were PP and PE.
Copyright (c) 2026 Aliya Ahmed Abdellah Ahmed, Shareefa Bint-e Umar, Khadeejah Qadir, Zehra S. Sharif (Author) https://creativecommons.org/licenses/by-nc/4.0/
Novel Insights into Preclinical Oncology: Can Blood-Based Genomics Predict Cancer Years in Advance ?
Cancer diagnosis at an early stage is essential to enhance prognosis since traditional diagnostic techniques usually detect the tumor at a late stage. The blood-based genomics such as circulating tumor DNA (ctDNA), cell-free DNA (cfDNA), and DNA methylation provide a less invasive solution to identify preclinically occurring malignancies. With ultra-sensitive sequencing and methylation-based assay, it is possible to detect cancer-specific molecular signatures in plasma, which can be used to detect multi-cancer early detection (MCED) with high specificity and moderate sensitivity. Fragmentomic profiling is also more predictive by considering the length of the fragments of the DNA and the pattern on the genomic structure, enabling accurate identification of the tissue-of-origin. Despite all issues still persisting, such as small ctDNA content in early tumors, technical and bioinformatics, cost and ethical issues on the detection of malignancy in non-symptomatic individuals. Genomic approaches targeting blood-based biomarkers would be a game changer in the oncology by presenting a golden opportunity of treating patients and saving their lives by providing early intervention.
Copyright (c) 2026 Ayisha Yousaf, Fatima Ali (Author) https://creativecommons.org/licenses/by-nc/4.0/
Copyright (c) 2026 Al-Najam Journal of Medical and Life Sciences https://creativecommons.org/licenses/by-nc/4.0/
Plant Cell Wall Engineering: Redefining Industrial Biomass through Molecular Innovation
Biomass, particularly lignocellulosic biomass, a promising renewable energy source in the production of biofuel and bio-based products, but its effective use is limited due to the cell wall recalcitrance. The intricate structure of the plant cell wall limits the enzymatic accessibility, which leads to the low conversion efficiency of less than 10% into fermentable sugars. Recent developments in molecular and genetic engineering, especially the CRISPR-Cas based genome editing and pathway manipulation, have enabled the targeted modifications of the cell wall components. Experimental results show that modifications of lignin biosynthesis and composition have the potential to increase saccharification efficiency without causing growth penalties. Cellulose crystallinity and hemicellulose structure modifications can enhance the digestibility of biomass. This review critically discusses the molecular basis of cell wall recalcitrance, recent experimental approaches to reduce the recalcitrance, and evaluates their industrial relevance in enhancing biomass conversion efficiency.
Copyright (c) 2026 Hafsa Aslam https://creativecommons.org/licenses/by-nc/4.0/
Mitochondrial DNA Mutations and Oxidative Phosphorylation Reprogramming in Colorectal Cancer and Breast Cancer: Systematic Review of Distinct Mitochondrial Mechanisms in Tumor Progressions
Background: Mitochondrial dysfunction with mitochondrial DNA (mtDNA) mutations and oxidative phosphorylation (OXPHOS) reprogramming have a significant role in cancer progression. The aim of the study was to mechanically compare different mechanisms of mitochondria in tumour development, both in breast and colorectal cancer. Methodology: It was a systematic review based on PRISMA guidelines 2020. The databases used in the search were PubMed, Scopus, Web of Science, and Google Scholar from 2020-2026. This was done by including clinical, experimental in vitro and in vivo studies that examined the role of mitochondrial DNA mutations and OXPHOS pathways in breast and colorectal cancer and excluding reviews, case reports, non-English studies, and irrelevant disease models. Newcastle-Ottawa Scale (NOS), Joanna Briggs Institute (JBI) checklist, ROBINS-I tool, modified in vitro tools, and SYRCLE tool were all used to assess risk of bias, with some certainty of evidence assessed using the GRADE framework. Results: 12 studies meet the inclusion criteria. Results have shown that OXPHOS reprogramming and the presence of the mutations in the mitochondrial DNA resulted in electron transport dysfunction, reactive oxygen species generation, and ATP production, all of which were contributing factors to tumour progression, metabolic adaptation, and therapeutic resistance. Mitochondrial pathways also had an effect on tumor microenvironment and prognosis. The risk of bias was moderate in general and the certainty of evidence was low according to GRADE assessment. Conclusion: Mitochondrial changes are the main focus of cancer development and are potential therapeutic targets. It is recommended that future research should be done on clinical validation and development of mitochondrial-targeted therapy to treat cancer on a personal basis.
Copyright (c) 2026 Naveera Mazhar, Maha Aslam khan, Arslan Majeed, Kainat Zafar (Author) https://creativecommons.org/licenses/by-nc/4.0/
Mitochondrial Dysfunction and Bioenergetic Instability in Cancer Pathogenesis: Systematic Review of Mitochondria-Targeted Therapeutic Approaches
Background: Mitochondrial dysfunction and bioenergetic instability play key roles in cancer pathogenesis. This study aimed to systematically evaluate the role of mitochondria-targeted interventions in breast, lung, and colorectal cancers. Methods: This systematic review followed PRISMA guidelines 2020. Databases searched included PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar, from 2020 to 2026. Experimental in vitro, in vivo, ex vivo, and clinical studies evaluating mitochondrial pathways or mitochondria-targeted interventions in breast, lung, and colorectal cancers were included, while reviews, editorials, case reports, conference abstracts, and non-English studies were excluded. Risk of bias was assessed using the SYRCLE tool, Cochrane Risk of Bias 2.0, and evidence certainty GRADE framework. Results: Twelve studies meet the inclusion criteria. Findings demonstrated that mitochondrial dysfunction, including OXPHOS inhibition, electron transport chain disruption, mitochondrial membrane depolarization, and ROS overproduction, contributed to tumor progression, chemoresistance, and metastasis. Mitochondria-targeted interventions reduced cancer cell viability, induced apoptosis, and improved treatment response. Risk of bias across studies was moderate, and the certainty of evidence was determined based on the GRADE approach. Conclusion: This review highlights the critical role of mitochondrial dysfunction in cancer progression and the potential of mitochondria-targeted therapies. Future research should focus on clinical translation, combination therapies, and molecular profiling to optimize patient-specific mitochondrial-based interventions.
Copyright (c) 2026 Ehsan Khan, Sabeeha Saddique, Syeda Maira Gillani, Sitara Ejaz, Sidra Anwar, Uday shree (Author) https://creativecommons.org/licenses/by-nc/4.0/
Molecular Insights into Adipokines in Metabolic Syndrome: Implications for Novel Therapeutic Strategies
Background: Adipokines are bio-active peptides released by adipose tissue which control glucose and lipid metabolism, play important roles in pathophysiology of metabolic syndrome (MetS). The main objective of this systematic review was to collect molecular evidence of adipokine dysregulation in MetS and fully evaluate its clinical, genetic, and epigenetic implications. Methodology: Articles published since January 2014 to January 2026 were searched from different databases like PubMed, Scopus, Web of Science, and Google Scholar, by following PRISMA 2020 guidelines. Inclusion criteria were adults, MetS, and quantitative data on adipokines and their association with clinical or genetic variables. The quality was measured using the Newcastle-Ottawa Scale, ROBINS-I tool, and GRADE frameworks. Results: 12 out of 85 records met the inclusion criteria. MetS populations were always associated with an increase in pro-inflammatory adipokines (leptin, resistin, chemerin, visfatin) and a decrease in adiponectin, which are strictly linked to insulin resistance and inflammation. The severity of MetS was more strongly associated with visceral adipose tissue expression as compared to circulating levels alone. Adiponectin and leptin genetic variations (e.g., ADIPOQ, 73 CpG) and epigenetic changes (211 CpGs) controlled the expression of adipokines. The quality was quite average, with observational designs making it hard to make causal inferences. Conclusion: The dysregulation of adipokines is the core of MetS pathophysiology with tissue-specific expression and epigenetic regulation being the factors involved in metabolic dysfunction. Long-term, multi-omics longitudinal studies are necessary in the future to confirm therapeutic targets and allow individual interventions.
Copyright (c) 2026 Kashaf Asghar, Muhammad Taimoor, Aqeel Ahmed, Hamdan Khalid (Author) https://creativecommons.org/licenses/by-nc/4.0/
Oxidative Stress, Mitochondrial Dysfunction, and Protein Misfolding Across Alzheimer’s, Parkinson’s, and Huntington’s Disease: A Systematic Review on Biomolecular Therapeutic Interventions
Background: Oxidative stress, mitochondrial dysfunction, and protein misfolding are some of the key and interrelated mechanisms in major neurodegenerative disorders. The purpose of this systematic review was to assess biomolecular therapeutic interventions of these pathways in the models of Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD). Methods: This is a systematic review that follow PRISMA 2020 guidelines. The searches took place up to from 2020 to 2026 in PubMed, Scopus, Web of Science, and Google Scholar. Experimental in vitro, in vivo, and ex vivo studies on biomolecular interventions that examine oxidative stress, mitochondrial dysfunction, or protein misfolding were accepted and reviews, editorials, conference abstracts, and non-English articles had been excluded. Screening and data extraction were done by two independent reviewers. The risk of bias was determined with the help of SYRCLE Risk of Bias tool of animal studies and Cochrane Risk of Bias 2.0 tool of in vitro studies and certainty of evidence was measured with the help of GRADE framework. Results: Twelve studies that passed the inclusion criteria were included following screening and eligibility. In disease models, interventions continually lowered the level of reactive oxygen species, restored mitochondrial bioenergetics, triggered Nrf2-mediated antioxidant response, lessened pathological protein aggregation, and neurobehavioral function. The risk of bias was low to moderate. Conclusion: The approach of the mitochondrial redox imbalance and proteostasis is a promising cross-disease treatment of neurodegeneration. To enhance the study further, future studies are needed to concentrate on standard experimental designs and clinical validation.
Copyright (c) 2026 Irshad Khan, Asad Khalid, Mujtaba Ehsan, Muhammad Akram, Ejaz Ehsan Khan, Khaleeq Ullah (Author) https://creativecommons.org/licenses/by-nc/4.0/
Plants Phytochemicals: Recovering Cancerous Cells
Cancer is a multifactorial disease of mammoth burden of global scale and the second major cause of death worldwide where millions of new cases are diagnosed each year 1. The cancer characteristics, such as long-term proliferative signaling, apoptotic resistance, invasion and metastasis, and immune destruction, are multifaceted therapeutic targets that cannot be adequately addressed by conventional therapeutic modalities like surgery, radiotherapy, and chemotherapy. The growing body of ethnopharmacological and molecular studies has recently shifted the focus to phytochemicals, which are secondary plant metabolites, as promising therapeutic agents in the recovery and reprogramming of cancerous cells 2. Phytochemicals are structurally heterogeneous bioactive substances that are produced by plants as elements of their adaptive defense systems. These molecules represent only a wide chemical distribution that comprise of phenolic acids, flavonoids, stilbenes, lignans, terpenoids, alkaloids, saponins and organosulfur compounds 3. Their anticancer action is not limited to cytotoxicity, but phytochemicals have multifaceted molecular negotiations with oncogenic signaling pathways, epigenetic modulators, and tumor microenvironment elements, which collectively tip the biological balance between a malignant and a quiescent or an apoptotic cellular state 4. The increasing in vitro, in vivo and preclinical evidence favors the therapeutic interest of phytochemicals in a wide variety of cancers, such as breast, colorectal, lung, hepatocellular, and prostate malignancies 5. Flavonoids and cell cycle arrest Flavonoids are a type of anticancer phytochemicals that are one of the best-researched classes of phytochemicals. Quercetin, kaempferol, luteolin and epigallocatechin-3-gallate (EGCG) have shown the ability to block cell cycle at the G1/S and G2/M checkpoints by regulating cyclins and cyclin-dependent kinases 6. These polyphenolic substances induce the expression of tumor suppressor proteins like p53 and p21, which provide molecular states that are hostile to the uncontrolled cell division. The role of flavonoids in the regulation of long non-coding RNA expression that regulates proliferative gene networks in colorectal and lung cancer cells has also been explained in recent studies 7. At the same time, flavonoids reduce the expression of antiapoptotic proteins such as Bcl-2 and Bcl-xL, and stimulate the induction of caspase-dependent apoptotic cascades. EGCG, a green tea extract, has shown specific ability to stimulate mitochondrial-pathway apoptosis in breast and prostate cancer by stimulating Bax and cytochrome c release 8. Notably, the most recent pharmacokinetic studies have discovered nanoencapsulation methods that can enhance the oral bioavailability of quercetin and kaempferol far beyond their established clinical translation shortcoming 9. NF-B pathway and terpenoids inhibition Another structurally diverse phytochemical group that has been shown to have anticancer activity is terpenoids. Triterpenoid including betulinic acid and ursolic acid induce apoptosis in cancer-causing cells but not normal tissue, which provides significant therapeutic benefit relative to traditional cytotoxic therapy 10. Sesquiterpene lactones, such as parthenolide and synthetic analogues, have been identified to inhibit nuclear factor-kappa B (NF- kB) pathway, which is a supreme controller of tumour survival, inflammatory crosstalk, and chemotherapy resistance. A study carried out in 2021 showed that parthenolide was able to sensitize triple-negative breast cancer cells to doxorubicin by disrupting antiapoptotic signalling orchestrated by NF-KB 11. NF-KB suppression by phytochemical therapies thus suppresses the expression of pro-survival cytokines, matrix metalloproteinases, and angiogenic factors which promote tumour growth (Figure 1). Recent in vivo models have demonstrated impaired Ras-MAP kinase signaling and lowered tumor burden in pancreatic and colorectal cancer xenografts with limonene and perillyl alcohol, monocyclic monoterpenes derived by citrus peel, supporting the mechanistic diversity of terpenoid anticancer action 12. PI3K/Akt/mTOR signaling axis modulation. The PI3K/Akt/mTOR pathway is a common dysregulated signalling pathway in human tumors and enhances cell survival, proliferation and reorganization of cancerous cellular metabolism. A number of phytochemicals have been reported to be strong agonists of this pathway. Resveratrol is a stilbene present in grapes and red berries that suppresses phosphorylation of Akt and subsequent mTORC1 activation thus limiting protein production and causing autophagy-mediated death in cancer lines 13. The main bioactive curcuminoid of Curcuma longa, curcumin, also inhibits Akt and mTOR signaling and at the same time stimulates AMP-activated protein kinase, shifting the cancer cell metabolism towards catabolic signaling pathways that cannot support malignant growth 14. The formulation innovations such as phospholipid complexes and self-emulsifying drug delivery systems have facilitated the clinical translation of curcumin, and Phase II clinical trials have shown favorable safety profiles, as well as initial evidence of tumor marker reduction in colorectal cancer patients 15. Phytochemicals and anti-angiogenic mechanisms The angiogenic pathway of tumours which attracts new vascularity to meet its oxygen and nutrient needs is a key target of therapy in oncology. Genistein, epigallocatechin gallate and thymoquinone, phytochemicals have been observed to prevent vascular endothelial growth factor (VEGF) expression and receptor tyrosine kinase activity effectively starving tumours of the blood supply needed to grow and metastatically spread 16. Nigella sativa yields thymoquinone, which has been studied with great intensity, with several papers demonstrating its ability to suppress hypoxia-inducible factor-1alpha (HIF-1 alpha), the major transcriptional regulator of VEGF in hypoxic tumour cores 17. These antiangiogenic effects of plant bioactives are complementary to the already available anti-VEGF pharmacological agents and have been shown to add to the effect of known antiangiogenic agents in preclinical tumor models, implying future clinical protocols would be complementary with current antiangiogenic therapies 18. Re-educating the tumor microenvironment The tumour microenvironment (TME) is an immunosuppressive niche that comprises regulatory T cells, myeloid-derived suppressor cells, cancer-associated fibroblasts and polarized M2 macrophages and together they inhibit antitumour immune responses. Recently, phytochemicals have been identified to be regulators of the TME, with the ability to remodel immunosuppressive immune cells into cytotoxic phenotypes. Sulforaphane, an isothiocyanate of cruciferous vegetables activates M1 macrophage polarisation and increases dendritic cell maturation, and thus, rescues immunosurveillance in the tumour milieu 19. Recent studies have shown that the berberine and luteolin inhibit the activation of cancer-associated fibroblasts and lower the release of tumour-promoting growth factors such as transforming growth factor- 20 and stromal cell-derived factor-1 20. Phytochemicals as epigenetic modulators A central element of the process of carcinogenesis is epigenetic dysregulation, which entails altered DNA-methylated states, histone-altered states, and non-coding RNA. Phytochemicals also have significant epigenetic modulatory properties, which provides a mechanism of gene expression normalisation to enhance direct cytotoxicity. EGCG is a DNA methyltransferase (DNMT) inhibitor, which reactivates tumour suppressor gene silenced in colorectal and breast cancers by promoter hypermethylation. One study has shown that inhibition of DNMT3a by EGCG could restore DKK3 Wnt antagonist expression in hepatocellular carcinoma and inhibit the expansion of tumors in vivo significantly 21. Curcumin suppresses histone deacetylases (HDACs) and increases acetylation of tumour suppressor gene loci that stimulate their transcriptional reinstatement. Moreover, resveratrol stimulates the action of Sirtuin-1 (SIRT1), a class III HDAC, which alters the acetylation levels of p53 and NF-kB and shifts their action towards tumour suppressive and not protective action 22. Together, these epigenetic activities have indicated that phytochemicals might be especially useful at reversing oncogenic epigenomic programming which presently represents a growing clinical goal due to the emerging epigenetic cancer therapy landscape 23. Hormonal control cancer and glucosinolates The Glucosinolates and hydrolysis products of glucosinolates, especially the indole-3-carbinol (I3C) and 3,3'-diindolylmethane (DIM) produced by Brassica species, have proven pleiotropic anticancer properties with particular application against hormonally-driven cancer. I3C alters oestrogen receptor signalling, favours the 2-hydroxylation of estradiol to the more genotoxic 16alpha-hydroxylation pathway and suppresses the expression of the oncogene HER2/neu in breast cancer models 24. In a 2021 clinical pilot study, DIM supplementation in women with early-stage cervical intraepithelial neoplasia had been found to achieve histological regression in a considerable proportion of participants over placebo, giving the preclinical supportive evidence on the hypothesized mechanism translational credibility 25. These phytochemicals comprise a mechanistically dissimilar group of anticancer agents that have been specifically employed in breast, cervical, and endometrial carcinomas, in which the hormonal disturbance contributes to tumor growth. In the future, further randomized controlled trials should determine the clinical dosing and efficacy parameters of them 26. CONCLUSION Plant phytochemicals are scientifically sound and diverse in mechanism bioactive molecules that have considerable potential in the re-covering of cancerous cells. Phytochemicals interact with malignant cellular biology at multiple points of vulnerability concurrently, by modulating apoptotic cascades, oncogenic signaling pathways, angiogenesis, epigenetic programming, immune microenvironmental dynamics as well as drug resistance mechanisms. The available preclinical evidence has shown persuading anticancer activities in a wide range of cancers and phytochemical families. The findings are increasingly being confirmed by translational clinical trials, but issues relating to bioavailability, standardization, and pharmacokinetic optimization still need to be overcome. Implementation of phytochemical-based interventions into a multidisciplinary oncology care is likely to revolutionize the therapeutic outcomes, treatment-related toxicity, and survival rates in cancer patients.
Copyright (c) 2026 Rameesha Ashraf (Author) https://creativecommons.org/licenses/by-nc/4.0/
Periodontal-Cardiometabolic Axis: How Oral Biology Shapes Critical Care Outcomes
Periodontal disease is among the most prevalent chronic inflammatory diseases globally, that is characterized by unremitting dysbiosis of microbes and destruction of tooth supportive tissue 1. Periodontitis is traditionally thought of as a localized oral disease but today is being perceived as a systemic inflammatory disease with extensive health consequences. The damaged periodontal pocket epithelium offers a direct pathway of entry of oral bacteria and their toxic by-products into the bloodstream leading to recurrent occurrences of bacteremia and systemic immune response 2. This unending microbial challenge is central in influencing the so called periodontal-cardiometabolic axis. Chronic periodontal inflammation favors the release of systemic inflammatory mediators such as interleukin-6, tumor necrosis factor-a and C-reactive protein that are highly implicated in endothelial dysfunction and atherogenesis 3. These circulating mediators destroy vascular homeostasis, diminish nitric oxide levels of bioavailability and increase oxidative stress to form a biological environment where cardiovascular disease is favorable. Most recent molecular and epidemiological findings indicated that moderate to severe periodontitis patients have a greater number of systemic inflammatory indicators and are at a higher risk of coronary artery disease and ischemic stroke 4. Oral microbial by-products have direct effects on cardiometabolic pathways in addition to having effects on inflammatory signaling. The major periodontal pathogens like Porphyromonas gingivalis and Fusobacterium nucleatum have the capability of spreading to the bloodstream and engaging with the endothelial cells in the vascular beds, macrophages and platelets 5. Gram-negative oral bacteria lipopolysaccharides initiate Toll-like receptor signaling and nuclear factor-kB signaling and stimulate chronic low-grade inflammation and rapid atherosclerotic plaque 6. The mechanistic proof that these biological mechanisms have in support of the part of oral microbiology in cardiovascular pathology is substantiated. The oral microbiome also interacts with the systemic metabolism in the oral-gut microbiota axis. New findings have shown that the gastrointestinal tract can be colonized by oral bacteria and restructure intestinal microbial colonies, which alters the generation of short-chain fatty acids structuring the bile acid metabolism and inflammatory metabolites 7. Such microbial crosstalk has been attributed to insulin resistance, dyslipidemia and metabolic syndrome, and thus, supports the correlation between periodontal disease and cardiometabolic dysfunction 8. A typical and two-way relationship is the case of diabetes mellitus and periodontal disease. Hyperglycemia affects the neutrophil activity, collagen metabolism and vascular integrity, making them the predisposing factors of periodontal disease and tissue erosion 9. Periodontal inflammation on the other hand enhances insulin resistance by maintaining systemic inflammatory load and disrupting the insulin signalling pathways 10. According to recent clinical data, a person with inadequately managed type 2 diabetes and active periodontitis is at higher risk of cardiovascular events and complications significantly than a metabolically healthy person 11. These are the biological interactions that are especially pertinent to the cases of critical illness. Inflammation on a systemic scale, loss of control over the immune system and metabolic imbalance are significant prognostic variables in intensive care units. Periodontal disease has the potential to add to the cumulative inflammatory burden and could enhance inflammatory responses in sepsis, acute cardiovascular events and metabolic decompensation 12. The similar levels of C-reactive protein and pro-inflammatory cytokines found in severe periodontitis and severely ill patients indicate similar inflammatory pathways that may exacerbate organ dysfunction and slow down the recovery process 13. The translocation of oral microbial organisms can also impact the intensive care outcomes through making the patients vulnerable to secondary infections and maladaptive immune activities. The poor oral hygiene and decreased salivary flow in critically unstable patients encourages the growth of oral microbes, which can act as a source of respiratory and systemic pathogens 14. Despite the limited number of direct interventional trials, recent narrative and clinical reviews indicate that poor oral health correlates with longer hospitalization, increased risk of infection and adverse recovery trajectories on vulnerable hospitalized populations 15. Understanding of the periodontal-cardiometabolic axis has led to the focus of the significance of combined medical and dental treatment. The beneficial effects of periodontal therapy on endothelial function, as well as the decrease of systemic inflammatory markers, have demonstrated that oral inflammation management could potentially help to reduce cardiometabolic risks on a broader level 16. Integrating oral health assessment into cardiometabolic and critical care interventions could thus be a significant and changeable practice to enhance patient outcome. In conclusion, cardiometabolic diseases are serious biological risks of periodontal disease through the process of chronic inflammation, microbial dysbiosis, and immune-metabolic interactions The existing literature shows that oral biology does have a significant role in the formation of cardiovascular risk, the control of diabetes, and possibly the results in intensive care. The introduction of periodontal care into multidisciplinary cardiometabolic and critical care systems has the potential to decrease systemic complications and aid in the long-term recovery of high-risk groups of patients.