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Abstract
Doxorubicin (DOX) is associated with cardiotoxicity due to its impact on various cellular processes.
- The mechanisms of DOX-induced cardiac injury include oxidative stress, inflammation, and cell death.
- Dysregulation of metal ion balance and mitochondrial dysfunction also contribute to cardiac damage.
- The p38 MAPK pathway plays a central role in integrating these damaging signals and influencing cell responses.
- Natural compounds may reduce DOX-induced cardiotoxicity by modulating p38 MAPK signaling.
- Sex-specific differences in cardioprotection are linked to distinct p38 MAPK isoforms.
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