ArticleCancer chemotherapy and pharmacology2025
A novel cardioprotective mechanism of rosuvastatin: restoring PINK1/parkin-mediated mitophagy via SIRT1/FOXO1 activation in doxorubicin-induced cardiotoxicity.
Article in Cancer chemotherapy and pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Experimental beneficial effect of rosuvastatin on burn wound healing in a rat model.World journal of experimental medicine · 2026Article
- The mechanisms and therapeutic advances of interactions between breast cancer and cardiovascular diseases.Frontiers in pharmacology · 2026Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemotherapy remains a key cancer treatment despite advancements in cancer therapy, with doxorubicin (DOX) widely used for solid and hematological tumors. However, its clinical use is limited by severe acute and chronic cardiotoxicity, primarily driven by oxidative stress and mitophagic dysregulation. Rosuvastatin (RSV), a lipid-lowering drug, has shown cardioprotective effects. This study aimed to investigate the molecular mechanism underlying RSV's protection against DOX-induced cardiotoxicity.
methodsAdult male Wistar rats were assigned to eight groups: control, RSV-only (20 mg/kg, orally, for 3 weeks), DOX-only (18 mg/kg, intraperitoneally, over 2 weeks), RSV + DOX, CQ + RSV + DOX (chloroquine 25 mg/kg, intraperitoneally, for 2 weeks), CQ-only, RSV + CQ, and CQ + DOX. 48 h after the last DOX injection, serum myocardial injury markers, oxidative stress markers, and autophagic flux biomarkers (LC3II & P62) were assessed. RT-PCR evaluated lncRNA APF gene expression, while western blotting quantified p-SIRT1, FOXO1, p-PINK1, and p-Parkin protein levels.
resultsRSV mitigated DOX-induced myocardial injury and oxidative stress while restoring autophagic flux, as evidenced by P62 and LC3II reversal. RSV enhanced lncRNA APF gene expression, p-SIRT1, p-PINK1, and p-Parkin levels while downregulating FOXO1. The autophagy inhibitor CQ blunted RSV's cardioprotective effects.
conclusionRSV protects against DOX-induced cardiotoxicity, at least in part, by restoring autophagic flux and rescuing PINK1/Parkin-mediated mitophagy via upregulation of the SIRT1/FOXO1 pathway. Thus, combining RSV with DOX may enable patients to complete chemotherapy with a reduced risk of cardiotoxicity. However, further studies are warranted to confirm its translational potential.
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Registered trials
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