ArticleFrontiers in endocrinology2022
Quercetin alleviates diastolic dysfunction and suppresses adverse pro-hypertrophic signaling in diabetic rats.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 14 citations in OpenAlex.
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- Chronic quercetin supplementation modulates cardiac function and signaling pathways in aged male Wistar rat hearts subjected to ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Article
- Impact of obesity on myocardial function and survival after cardiac arrest and cardiopulmonary resuscitation in a rat model.Scientific reports · 2025Article
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- A comprehensive review on diabetic cardiomyopathy (DCM): histological spectrum, diagnosis, pathogenesis, and management with conventional treatments and natural compounds.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- HDAC4: an emerging target in diabetes mellitus and diabetic complications.European journal of medical research · 2025Review
- Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025Review
- Sea buckthorn flavonoids and their derivatives: potential natural compounds for the treatment of diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Multi-omics insights into the pathogenesis of diabetic cardiomyopathy: epigenetic and metabolic profiles.Epigenomics · 2025Article
- Role of Quercetin in Diabetic Cardiomyopathy.Plants (Basel, Switzerland) · 2024Review
- Mitigating Doxorubicin-Induced Cardiotoxicity through Quercetin Intervention: An Experimental Study in Rats.Antioxidants (Basel, Switzerland) · 2024Article
- A Review on the Natural Products in Treatment of Diabetic Cardiomyopathy (DCM).Reviews in cardiovascular medicine · 2024Review
- Update on clinical and experimental management of diabetic cardiomyopathy: addressing current and future therapy.Frontiers in endocrinology · 2024Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Quercetin (Que) is a potent anti-inflammatory and antioxidant flavonoid with cardioprotective potential. However, very little is known about the signaling pathways and gene regulatory proteins Que may interfere with, especially in diabetic cardiomyopathy. Therefore, we aimed to study the potential cardioprotective effects of Que on the cardiac phenotype of type 2 diabetes mellitus (T2DM) accompanied by obesity. Methods: For this experiment, we used Zucker Diabetic Fatty rats (fa/fa) and their age-matched lean controls (fa/+) that were treated with either vehicle or 20 mg/kg/day of Que for 6 weeks. Animals underwent echocardiographic (echo) examination before the first administration of Que and after 6 weeks. Results: After the initial echo examination, the diabetic rats showed increased E/A ratio, a marker of left ventricular (LV) diastolic dysfunction, in comparison to the control group which was selectively reversed by Que. Following the echo analysis, Que reduced LV wall thickness and exhibited an opposite effect on LV luminal area. In support of these results, the total collagen content measured by hydroxyproline assay was decreased in the LVs of diabetic rats treated with Que. The follow-up immunoblot analysis of proteins conveying cardiac remodeling pathways revealed that Que was able to interfere with cardiac pro-hypertrophic signaling. In fact, Que reduced relative protein expression of pro-hypertrophic transcriptional factor MEF2 and its counter-regulator HDAC4 along with pSer Discussion: In summary, we showed for the first time that Que ameliorated pro-hypertrophic signaling on the level of epigenetic regulation and targeted specific upstream pathways which provoked inhibition of pro-hypertrophic signals in ZDF rats. Moreover, Que mitigated T2DM and obesity-induced diastolic dysfunction, therefore, might represent an interesting target for future research on novel cardioprotective agents.
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