Quercetin and Cardiovascular Health: An Evidence‐Based Review of Risk Factors and Treatments
- 1Cardiovascular Diseases Research Center Birjand University of Medical Sciences Birjand Iran.
- 2Department of Clinical Pharmacy, School of Pharmacy Birjand University of Medical Sciences Birjand Iran.
- 3Student Research Committee Birjand University of Medical Sciences Birjand Iran.
Abstract
Cardiovascular diseases (CVD) encompass a variety of conditions, including coronary heart disease, peripheral arterial disease, cerebrovascular disease, rheumatic heart disease, and venous thromboembolism. Natural products exhibit a range of pharmacological activities, including antioxidant, anti-inflammatory, and immunoregulatory effects. This review evaluates the potential therapeutic effects of quercetin on factors contributing to cardiovascular disease risk. Quercetin, a flavonoid recognized for its strong antioxidant capabilities, has demonstrated beneficial effects in alleviating pathological cardiac conditions such as hypertrophy and ischemia across multiple in vitro and in vivo experimental models. This review compiles evidence demonstrating quercetin's ability to reduce cardiac hypertrophy and apoptosis in cardiomyocytes through modulation of key signaling pathways. Specifically, quercetin treatment resulted in significant upregulation of protective proteins such as silent information regulatory factor 1 (SIRT1), peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), and Bcl-2, coupled with downregulation of pro-apoptotic Bax. Quercetin improved calcium channel function, enhanced myocardial contractility, and decreased oxidative stress markers, leading to improved survival rates of cardiomyocytes under ischemic conditions. Quercetin administration has been shown to lower systolic and diastolic blood pressure and reduce cardiac hypertrophy. Additionally, quercetin positively influences lipid profiles by decreasing total cholesterol, triglycerides, and low-density lipoprotein while enhancing overall lipid metabolism. Collectively, these findings highlight quercetin as a promising candidate in preclinical models of cardiac hypertrophy and ischemia. However, further research-particularly well-designed clinical trials-is essential to validate these findings and determine the translational potential through dietary interventions of quercetin in human cardiovascular health.
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BibTeX
@article{khazdair2026quercetin,
title = {{Quercetin and Cardiovascular Health: An Evidence‐Based Review of Risk Factors and Treatments}},
author = {Mohammad Reza Khazdair and Shima Jafari and Melika Shoghi},
journal = {Food science \& nutrition},
year = {2026},
month = oct,
doi = {10.1002/fsn3.72514},
url = {https://europepmc.org/article/PMC/PMC13717219},
note = {CC BY},
}
RIS
TY - JOUR
TI - Quercetin and Cardiovascular Health: An Evidence‐Based Review of Risk Factors and Treatments
AU - Mohammad Reza Khazdair
AU - Shima Jafari
AU - Melika Shoghi
PY - 2026
DA - 2026/10/28
JO - Food science & nutrition
DO - 10.1002/fsn3.72514
UR - https://europepmc.org/article/PMC/PMC13717219
AB - Cardiovascular diseases (CVD) encompass a variety of conditions, including coronary heart disease, peripheral arterial disease, cerebrovascular disease, rheumatic heart disease, and venous thromboembolism. Natural products exhibit a range of pharmacological activities, including antioxidant, anti-inflammatory, and immunoregulatory effects. This review evaluates the potential therapeutic effects of quercetin on factors contributing to cardiovascular disease risk. Quercetin, a flavonoid recognized for its strong antioxidant capabilities, has demonstrated beneficial effects in alleviating pathological cardiac conditions such as hypertrophy and ischemia across multiple in vitro and in vivo experimental models. This review compiles evidence demonstrating quercetin's ability to reduce cardiac hypertrophy and apoptosis in cardiomyocytes through modulation of key signaling pathways. Specifically, quercetin treatment resulted in significant upregulation of protective proteins such as silent information regulatory factor 1 (SIRT1), peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), and Bcl-2, coupled with downregulation of pro-apoptotic Bax. Quercetin improved calcium channel function, enhanced myocardial contractility, and decreased oxidative stress markers, leading to improved survival rates of cardiomyocytes under ischemic conditions. Quercetin administration has been shown to lower systolic and diastolic blood pressure and reduce cardiac hypertrophy. Additionally, quercetin positively influences lipid profiles by decreasing total cholesterol, triglycerides, and low-density lipoprotein while enhancing overall lipid metabolism. Collectively, these findings highlight quercetin as a promising candidate in preclinical models of cardiac hypertrophy and ischemia. However, further research-particularly well-designed clinical trials-is essential to validate these findings and determine the translational potential through dietary interventions of quercetin in human cardiovascular health.
SN - 2048-7177
ER -