Kielin/chordin-like protein(KCP) deficiency exacerbates doxorubicin-induced myocardial injury by promoting macrophage M1 polarization through autophagy inhibition.

Yibo Wang, Qingwei Ji, Liren Gan, Yongqi Feng, Heng Pan, Xiyi Lu, Jing Ye, Lingyue Qiu, Qingkuan Li, Jianwei Zhang, Jun Wan, Yuan Wang, Di Ye

Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan, 430060, China.Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan, 430060, China. · pubmed

Paper

Abstract

KCP has been demonstrated to be involved in cardiac remodeling and cardiac aging. This study aims to investigate whether KCP plays a regulatory role in doxorubicin (DOX)-induced cardiac injury by modulating immune and inflammatory responses.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

KCP deficiency exacerbates doxorubicin-induced myocardial injury by promoting macrophage M1 polarization through autophagy inhibition. The study investigates a potential regulatory role of KCP in cardiac injury, which is relevant to understanding mechanisms of cardiac aging and inflammation, contributing to the broader context of age-related diseases.

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