Cardioprotective effects of naringin, hesperidin, and hesperetin: modulation of atherosclerosis, cardiac remodeling, and myocardial ischemia/infarction.

Cardiovascular diseases (CVDs) persist as the predominant contributor to morbidity and mortality on a global scale, principally attributed to the pathophysiological processes of atherosclerosis, cardiac remodeling, and myocardial ischemia/infarction. Contemporary research underscores the cardioprotective efficacy of natural flavonoids, including naringin, hesperidin (HES), and hesperetin (HST), bioactive constituents prevalent in citrus fruits. These flavonoids demonstrate multifaceted effects, encompassing antioxidant, anti-inflammatory, anti-apoptotic, lipid-lowering, and endothelial-protective properties, all of which synergistically enhance cardiovascular performance. At the molecular nexus, naringin, HES, and HST influence critical signaling pathways, thus diminishing oxidative stress, obstructing the action of inflammatory cytokines, and curtailing the proliferation of vascular smooth muscle cells. Furthermore, these bioactive compounds regulate cardiac remodeling by alleviating fibrosis, hypertrophy, and mitochondrial dysfunction, whilst simultaneously promoting angiogenesis and optimizing energy metabolism. In experimental models of myocardial ischemia and infarction, they facilitate cardiomyocyte viability and diminish infarct size through the modulation of apoptosis-related genes and the mitigation of oxidative injury. This review meticulously synthesizes the mechanistic insights and preclinical data that substantiate the cardioprotective properties of naringin, HES, and HST. Additionally, it examines their pharmacokinetic profiles, bioavailability, and prospective clinical applications as adjunctive agents in the prophylaxis and management of CVDs. Elucidating these molecular pathways could offer a promising framework for the formulation of predictive, preventive, and personalized strategies aimed at combatting CVDs.