Medicine and Health

Acyl-CoA thioesterase 1 prevents cardiomyocytes from Doxorubicin-induced ferroptosis via shaping the lipid composition

Y. Liu, L. Zeng, et al.

This study explores the crucial role of Acyl-CoA thioesterase 1 (Acot1) in doxorubicin-induced cardiotoxicity, shedding light on how its regulation could protect against ferroptosis in heart cells. Conducted by Yunchang Liu and colleagues, the research points to Acot1 as a promising therapeutic target for preventing damage caused by chemotherapy.

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Abstract

This study investigated the role of Acyl-CoA thioesterase 1 (Acot1) in doxorubicin-induced cardiotoxicity (DIC). Using C57BL/6 mice and HL-1 cardiomyocytes, the researchers confirmed that doxorubicin induces ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation. RNA sequencing revealed downregulation of Acot1 in DOX-treated murine hearts. Both in vitro and in vivo experiments demonstrated that Acot1 downregulation sensitizes cardiomyocytes to ferroptosis, while Acot1 overexpression protects against it. The protective effect of Acot1 appears linked to its role in shaping lipid composition, particularly influencing levels of docosahexaenoic acid (DHA). The study suggests that Acot1 could be a potential therapeutic target for preventing DIC.

Publisher

Cell Death and Disease

Published On

Sep 15, 2020

Authors

Yunchang Liu, Liping Zeng, Yong Yang, Chen Chen, Daowen Wang, Hong Wang

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