Mechanisms of RSV-targeted SIRT1 in the treatment of CVDs.
| RSV-targeted SIRTS | Mechanisms of action | Regulation of substrates and pathways | Roles in diseases | Research objects | References |
|---|---|---|---|---|---|
| SIRT1 | ↑SIRT1↓FOXO1 acetylation↓Bim | RSV enhances SIRT1 deacetylase activity, leading to decreased acetylation of FOXO1 and subsequent downregulation of the pro-apoptotic protein Bim. | Inhibits the apoptosis of myocardial cells and protects against cardiac aging and age-related cardiac dysfunction. | Male senescence-accelerated mice prone mice | [102] |
| SIRT1 | ↑SIRT1↓p53 acetylation↓Ferroptosis-related genes↓Lipid peroxidation | RSV activates SIRT1 deacetylase activity, thereby inhibiting cardiomyocyte ferroptosis and reducing lipid peroxidation stress. | Attenuates cardiomyocyte ferroptosis and decelerates heart failure progression. | C57BL/6 mice;Human-induced pluripotent stem cell-derived cardiomyocytes | [103] |
| SIRT1 | ↑SIRT1↓TGF-β1↓p-Smad3 | RSV restores SIRT1 function suppressed by pressure overload, thereby suppressing TGF-β1/Smad3-mediated programs of cardiac hypertrophy and fibrosis. | Attenuates pressure overload-induced cardiac hypertrophy and fibrosis. | Rat;NCMs | [104] |
| SIRT1 | ↑SIRT1↓PGC-1α/NRF-1/NRF-2 /TFAM↑Mitochondrial↑ATP/↓ROS | RSV activates SIRT1 to deacetylate PGC-1α and improve mitochondrial function in diabetic cardiomyopathy. | Alleviates cardiac dysfunction in diabetic cardiomyopathy by preserving mitochondrial function and energy metabolism. | SIRT1flox5-6/flox5-6;Myh6-Cre+ transgenic mice;H9c2 cardiomyoblast cell;H9c2 embryonic rat heart-derived cell | [105] |
| SIRT1 | ↑SIRT1↑NRF2↑Antioxidant gene↓ROS | RSV synergizes with FGF1 to activate SIRT1-NRF2 signaling and enhance antioxidant defense. | Attenuates doxorubicin-induced cardiotoxicity by reducing oxidative stress and improving cardiac function. | C57BL/6J male mice;H9c2 cardiomyoblast cell | [106] |
Bim: Bcl-2-interacting mediator of cell death; CVDs: cardiovascular diseases; FGF1: fibroblast growth factor 1; FOXO1: forkhead box O1; NCMs: neonatal rat cardiomyocytes; NRF2: nuclear factor erythroid 2-related factor 2; p53: tumor protein p53; PGC-1α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; p-Smad3: phosphorylated Sma- and mad-related protein 3; ROS: reactive oxygen species; RSV: resveratrol; SIRT: sirtuin; TFAM: mitochondrial transcription factor A; TGF-β: transforming growth factor-β.
JY: Data curation, Formal analysis, Investigation, Methodology, Writing—original draft, Writing—review & editing. SC: Data curation, Formal analysis, Investigation, Methodology, Writing—original draft, Writing—review & editing. TZ: Data curation, Formal analysis, Investigation, Methodology, Writing—original draft, Writing—review & editing. YZ: Data curation, Formal analysis, Investigation, Methodology, Writing—original draft, Writing—review & editing. ZL: Data curation, Formal analysis, Investigation, Methodology, Writing—original draft, Writing—review & editing. HL: Conceptualization, Investigation, Writing—review & editing, Supervision. All authors read and approved the submitted version.
The authors declare that there are no conflicts of interest.
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This work was supported by a grant from the Natural Science Foundation of Shandong Province, China [No. ZR2025MS387]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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