Key result
Quercetin offers promising cardioprotection in diabetic cardiomyopathy by targeting oxidative stress, inflammation, fibrosis, and apoptosis.
Why the study?
Diabetic cardiomyopathy is a severe, increasingly prevalent complication of diabetes, and understanding the mechanisms underlying quercetin's cardioprotective effects could inform future drug discovery efforts.
Does quercetin mitigate the progression of diabetic cardiomyopathy in diabetic models?
Does quercetin mitigate the progression of diabetic cardiomyopathy in diabetic models?
This review highlights the potential of quercetin as a therapeutic agent for diabetic cardiomyopathy by summarizing its multi-target cardioprotective mechanisms.
Quercetin shows promise against diabetic cardiomyopathy pathways; leaves open clinical translation pending prospective trials.
Diabetic cardiomyopathy is a significant and severe complication of diabetes that affects a large portion of the global population, with its prevalence continuing to rise. Secondary metabolites, including quercetin, have shown promising effects in mitigating the progression of diabetic cardiomyopathy by targeting multiple pathological mechanisms, including impaired insulin signaling, glucotoxicity, lipotoxicity, oxidative stress, inflammation, fibrosis, apoptosis, autophagy, mitochondrial dysfunction, cardiac stiffness, and disrupted calcium handling. Addressing these mechanisms is crucial to prevent left ventricular diastolic and systolic dysfunction in advanced stages of diabetic heart disease. Scientific evidence has highlighted the cardioprotective properties of quercetin at both the myocardial and cellular/molecular levels in diabetic models. Therefore, this review aims to present a comprehensive overview of the proposed mechanisms underlying quercetin's beneficial effects, providing valuable insights that could inform future drug discovery efforts specific to diabetic cardiomyopathy.
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Mustafa et al. (2024) conducted a review in Diabetic Cardiomyopathy. Quercetin was evaluated. Quercetin demonstrates promising cardioprotective effects in diabetic cardiomyopathy by targeting multiple pathological mechanisms including oxidative stress, inflammation, fibrosis, and apoptosis.
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