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All Journal Open Access Indonesian Journal of Medical Reviews
Tri Nisdian Wardiah
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Health Professions Medicine & Pharmacology

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eNOS, Cardiac Senescence, and Cardiovascular Aging: A Meta-Analysis of Molecular Mechanisms and Clinical Outcomes Tri Nisdian Wardiah; Ali Zainal Abidin; Taufik Indrajaya; Nur Riviati
Open Access Indonesian Journal of Medical Reviews Vol. 4 No. 6 (2024): Open Access Indonesian Journal of Medical Reviews
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/oaijmr.v4i6.685

Abstract

Endothelial nitric oxide synthase (eNOS) plays a critical role in maintaining cardiovascular homeostasis. Its dysfunction is implicated in cardiac senescence, a hallmark of aging characterized by cellular decline and increased risk of cardiovascular disease. This meta-analysis investigated the association between eNOS, cardiac senescence, and cardiovascular aging, exploring underlying molecular mechanisms and clinical outcomes. A systematic search of PubMed, Scopus, and Web of Science databases was conducted for relevant studies published between 2013 and 2024. Studies investigating the relationship between eNOS, cardiac senescence markers (e.g., telomere length, p53, p16), and cardiovascular outcomes (e.g., heart failure, myocardial infarction, stroke) were included. Data were extracted and pooled using random-effects models. Nine studies (n=4,875 participants) met the inclusion criteria. Meta-analysis revealed a significant association between reduced eNOS activity and increased cardiac senescence markers (standardized mean difference [SMD] = -0.85; 95% confidence interval [CI], -1.20 to -0.50; p<0.001). Furthermore, eNOS dysfunction was associated with an increased risk of cardiovascular events (relative risk [RR] = 1.62; 95% CI, 1.25 to 2.10; p=0.001). Molecular analysis indicated that eNOS dysfunction contributes to cardiac senescence through increased oxidative stress, inflammation, and impaired autophagy. In conclusion, this meta-analysis provides compelling evidence for the detrimental role of eNOS dysfunction in cardiac senescence and cardiovascular aging. Targeting eNOS may offer promising therapeutic strategies to mitigate age-related cardiovascular decline.
Targeting Interleukin-6 Signaling with Tocilizumab in Atherosclerosis: A Meta-Analysis of Anti-Inflammatory Effects and Plaque Stabilization Ali Zainal Abidin; Tri Nisdian Wardiah; Taufik Indrajaya; Nur Riviati
Open Access Indonesian Journal of Medical Reviews Vol. 5 No. 1 (2025): Open Access Indonesian Journal of Medical Reviews
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/oaijmr.v5i1.686

Abstract

Atherosclerosis, a chronic inflammatory disease, is the leading cause of cardiovascular disease. Interleukin-6 (IL-6) plays a crucial role in atherogenesis, making it a potential therapeutic target. Tocilizumab, an IL-6 receptor antagonist, has shown promise in reducing inflammation and stabilizing atherosclerotic plaques. This meta-analysis aimed to evaluate the efficacy and safety of tocilizumab in atherosclerosis by analyzing its impact on inflammatory markers and plaque characteristics. A systematic search of PubMed, Embase, and Cochrane Central Register of Controlled Trials was conducted from January 2013 to January 2024. Studies evaluating the effects of tocilizumab on inflammatory markers and plaque characteristics in patients with atherosclerosis were included. Randomized controlled trials (RCTs) and observational studies with a comparative arm were eligible. Data were extracted and pooled using a random-effects model. Nine studies (n=1248 participants) met the inclusion criteria. Tocilizumab significantly reduced CRP levels (standardized mean difference [SMD] -1.23; 95% confidence interval [CI] -1.56 to -0.90; p<0.001) and IL-6 levels (SMD -0.87; 95% CI -1.12 to -0.62; p<0.001) compared to control groups. A significant reduction in plaque volume (SMD -0.45; 95% CI -0.71 to -0.19; p=0.001) and an increase in fibrous cap thickness (SMD 0.38; 95% CI 0.12 to 0.64; p=0.004) were also observed. No significant increase in adverse events was reported in the tocilizumab group. This meta-analysis demonstrates that tocilizumab effectively reduces inflammation and promotes plaque stabilization in atherosclerosis. These findings suggest that tocilizumab may be a promising therapeutic strategy for preventing cardiovascular events in patients with atherosclerosis. Further large-scale RCTs are needed to confirm these findings and establish the long-term safety and efficacy of tocilizumab in this population.
Co-Authors Ali Zainal Abidin Nur Riviati, Nur Taufik Indrajaya