Inhibition of miR-23a attenuates doxorubicin-induced mitochondria-dependent cardiomyocyte apoptosis by targeting the PGC-1 α/Drp1 pathway.

CONCLUSIONS AND IMPLICATIONS: Increased miR-23a promoted mitochondrial injury in the Dox-induced cellular model. Inhibition of miR-23a attenuated cardiomyocyte damage by directly targeting PGC-1α/p-Drp1, thereby inhibiting mitochondria-dependent apoptosis. These findings may provide a new potential target for the treatment of Dox-induced cardiotoxicity.
PMID: 30831132 [PubMed - as supplied by publisher]

Source: Toxicology and Applied Pharmacology - February 28, 2019 Category: Toxicology Authors: Du J, Hang P, Pan Y, Feng B, Zheng Y, Chen T, Zhao L, Du Z Tags: Toxicol Appl Pharmacol Source Type: research