Key result
SGLT2 inhibitors emerge as the most clinically developed cardioprotective strategy against doxorubicin-induced cardiotoxicity.
Why the study?
Do emerging cardioprotective strategies such as SGLT2 inhibitors, repurposed drugs, and mitochondrial-targeted therapies prevent doxorubicin-induced cardiotoxicity compared to or beyond dexrazoxane?
Do emerging cardioprotective strategies such as SGLT2 inhibitors, repurposed drugs, and mitochondrial-targeted therapies prevent doxorubicin-induced cardiotoxicity compared to or beyond dexrazoxane?
This review highlights SGLT2 inhibitors as the most promising and clinically developed emerging cardioprotective strategy against doxorubicin-induced cardiotoxicity, offering a mechanistically integrative alternative to dexrazoxane.
Answers are grounded in this paper and cite their sources.
Mitochondrial dysfunction may drive DOX cardiotoxicity; leaves open whether SGLT2 inhibitor repurposing confers clinical benefit.
Doxorubicin (DOX) remains a foundation of cancer treatment; however, its clinical utility is seriously restricted by measurements of subordinate and frequently irreversible cardiotoxicity. In spite of the fact that dexrazoxane is as of now the as it were affirmed cardioprotective specialist, its limited viability and clinical restrictions highlight the require for elective methodologies. Developing prove shows that DOX-induced cardiotoxicity could be a systems-level clutter driven essentially by mitochondrial brokenness, metabolic resoluteness, disabled quality control, and controlled cell passing pathways. This audit fundamentally looks at rising cardioprotective methodologies past dexrazoxane, with a center on sodium glucose cotransporter 2 (SGLT2) inhibitors, medicate repurposing approaches, and mitochondrial-targeted treatments. We synthesize unthinking bits of knowledge and translational prove to compare these techniques in terms of robotic breadth and clinical status. SGLT2 inhibitors rise as the most clinically developed and robotically integrator choice, though repurposed drugs and mitochondrial-directed mediations offer complementary but variable potential. Finally, we highlight future bearings emphasizing combination treatments and accuracy cardioprotection to realize solid cardiac conservation in anthracycline-treated patients.
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Basirpour et al. (2026) conducted a review in Doxorubicin-induced cardiotoxicity. SGLT2 inhibitors, drug repurposing, and mitochondrial-targeted treatments was evaluated. SGLT2 inhibitors emerge as the most clinically developed cardioprotective strategy against doxorubicin-induced cardiotoxicity, while repurposed drugs and mitochondrial therapies offer variable potential.
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