Why the study?
Endothelial dysfunction contributes to impaired vasodilation, altered hemodynamics, and atherosclerosis, and this review aimed to elucidate the mechanisms of trimetazidine and its therapeutic potential for endothelial dysfunction and associated cardiovascular disorders.
Does trimetazidine improve endothelial dysfunction and related metabolic, oxidative, inflammatory, and atherosclerotic parameters in patients and models with cardiovascular diseases?
Does trimetazidine improve endothelial dysfunction and related metabolic, oxidative, inflammatory, and atherosclerotic parameters in patients and models with cardiovascular diseases?
This narrative review highlights the multifaceted preclinical and clinical mechanisms by which the antianginal agent trimetazidine improves endothelial dysfunction—via enhanced vasodilation, improved glucose metabolism, and reduced oxidative stress, inflammation, and atherosclerosis—supporting its potential for broader therapeutic translation in cardiovascular disease.
Answers are grounded in this paper and cite their sources.
May extend trimetazidine beyond angina for endothelial dysfunction; leaves open randomized confirmation in cardiovascular disease.
Endothelial dysfunction is a hallmark of cardiovascular diseases, contributing to impaired vasodilation, altered hemodynamics, and atherosclerosis progression. Trimetazidine, traditionally used for angina pectoris, exhibits diverse therapeutic effects on endothelial dysfunction. This review aims to elucidate the mechanisms underlying trimetazidine's actions and its potential as a therapeutic agent for endothelial dysfunction and associated cardiovascular disorders. Trimetazidine enhances vasodilation and hemodynamic function by modulating endothelial nitric oxide synthase activity, nitric oxide production, and endothelin-1. It also ameliorates metabolic parameters, including reducing blood glucose, mitigating oxidative stress, and dampening inflammation. Additionally, trimetazidine exerts antiatherosclerotic effects by inhibiting plaque formation and promoting its stability. Moreover, it regulates apoptosis and angiogenesis, fostering endothelial cell survival and neovascularization. Understanding trimetazidine's multifaceted mechanisms underscores its potential as a therapeutic agent for endothelial dysfunction and associated cardiovascular disorders, warranting further investigation for clinical translation.
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Kamisah et al. (2024) studied this question.
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