Research progress on cardiovascular protective mechanism of resveratrol.
10.19540/j.cnki.cjcmm.20250213.703
- Author:
Qian WU
1
;
Hui-Min LI
2
;
Chun-Kun YANG
3
;
Ying-Tian YANG
1
;
Shi-Han WANG
1
Author Information
1. Department of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing 100053, China.
2. Department of Traditional Chinese Medicine, Renmin Hospital of Wuhan University Wuhan 430060, China.
3. Department of Cardiology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine Ji'nan 250011, China.
- Publication Type:English Abstract
- Keywords:
cardiovascular diseases;
ischemia-reperfusion injury;
mechanisms;
oxidative stress;
resveratrol
- MeSH:
Humans;
Resveratrol/pharmacology*;
Animals;
Cardiotonic Agents/pharmacology*;
Oxidative Stress/drug effects*;
Cardiovascular Diseases/genetics*;
Cardiovascular System/metabolism*;
Signal Transduction/drug effects*
- From:
China Journal of Chinese Materia Medica
2025;50(12):3244-3251
- CountryChina
- Language:Chinese
-
Abstract:
Resveratrol(Res) is a kind of polyphenolic compound, possessing multiple biological activities such as antioxidant, anti-inflammatory, cardioprotective, and anticancer effects. In recent years, the cardiovascular protective mechanism of Res has become a research hotspot. Studies have shown that Res has a protective effect on the cardiovascular system through various pathways, such as inhibiting oxidative stress, regulating ferroptosis of cells, improving ischemia-reperfusion(I/R) injury, regulating lipid metabolism, suppressing inflammatory responses, and enhancing endothelial function. It can also alleviate cardiotoxicity caused by drugs and chemicals. In terms of oxidative stress, Res reduces the level of intracellular reactive oxygen species(ROS) by enhancing the expression of proteins such as silent information regulator 1(SIRT1) and regulating mitochondrial function, thereby alleviating myocardial cell damage. Regarding ferroptosis, Res inhibits the occurrence of ferroptosis by regulating the expression of proteins related to iron metabolism. Res can also improve I/R injury through mechanisms such as activating autophagy and the mitochondrial quality control network. In regard to improving endothelial function, Res protects the function of endothelial cells by regulating multiple signaling pathways, such as downregulating the PREP1-mediated pathway. Res can also regulate lipid metabolism and inhibit the progression of atherosclerosis. In terms of inflammatory responses, Res exerts anti-inflammatory effects through mechanisms such as inhibiting the nuclear factor-kappa B(NF-κB) signaling pathway. In addition, Res has an improving effect on cardiotoxicity caused by different drugs or environmental factors. However, the clinical application of Res still faces limitations such as poor pharmacokinetic properties. In the future, in-depth exploration is needed at multiple levels from basic research to clinical application to clarify the dose-response relationship and standardize the standards of medication regimens with the expectation of providing more effective strategies for the prevention and treatment of cardiovascular diseases.
