Sotagliflozin ameliorates doxorubicin-induced cardiomyopathy by regulating inflammation and mitochondrial dysfunction through the AMPK/mTOR pathway
Abstract
loading were reduced. Mitochondrial dysfunction was also improved, as indicated by increased JC-1 aggregates and Bcl-2/Bax ratios. Notably, SOTA activated 5' AMP-activated protein kinase (AMPK) and inhibited mTOR signaling while protecting from DOX-induced cardiomyopathy, suggesting SOTA as a promising therapeutic for heart failure treatment.
Fields of Study & Subjects
Chemotherapy-induced cardiotoxicity and mitigation
Metabolism
Diabetes
and Cancer
Cardiovascular Function and Risk Factors
Publication details
- Journal / source
- Experimental and Therapeutic Medicine
- Publisher
- Spandidos Publications
- Volume
- 32
- Issue
- 2
- Pages
- 1–18
- Publication date
- 4 June 2026
- Language
- EN