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For instance, chronic doxorubicin (DOX) intervention can also lead to cardiomyocyte aging, suggesting that the aging mechanism shares many irreversible stress factors with the cardiac injury pathway, such as decreased Sirtuins expression, increased p38 mitogen-activated protein kinases (p38MAPK) signaling, and decreased antioxidant enzyme levels represented by MnSOD [21, 22]

Current evidence remains exploratory, with no approved human applications, positioning the neurological research surrounding BPC-157 and neural repair as preliminary but consistently documented across animal models