Doxorubicin induces cardiotoxicity by enhancing autophagy via mTOR signaling in hiPSC- and hESC-derived cardiomyocytes.

ABSTRACT:

Introduction

Doxorubicin (DOX) is a highly effective anti-cancer drug, but its clinical applications are limited by its cardiotoxicity. The mechanisms underlying DOX-induced cardiotoxicity (DIC) remain incompletely understood. Human induced pluripotent stem cells (hiPSCs) and human embryonic stem cells (hESCs) offer an advanced platform for investigating DIC, as they accurately recapitulate human cardiac physiology and pathology. However, the roles and mechanisms of DIC in hiPSC-CMs and hESC-CMs, especially regarding autophagy dynamics and regulation, are still not well-defined.

Methods

Cell viability, apoptosis, reactive oxygen species production, and DNA damage were assessed. Autophagy was evaluated by transmission electron microscope, LC3-II/LC3-I ratio, and autophagy flu

SUBMITTER: Ke M 

PROVIDER: S-EPMC12685840 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature