SIRT5 Ameliorates Cardiac Fibrosis via PCK2 Desuccinylation-Mediated Metabolic Reprogramming in Cardiac Fibroblasts.

Maoxiong Wu, Jing Tan, Weibin Zhou, Zenghui Zhang, Qingyuan Gao, Yangwei Cai, Guanghong Liao, Zhengyu Cao, Chuanrui Zeng, Yi Zhang, Zhiteng Chen, Qiong Qiu, Zhaoyu Liu, Jingfeng Wang, Haifeng Zhang, Yangxin Chen

Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China. (M.W., W.Z., Z.Z., Q.G., Yangwei Cai, G.L., Z. Cao, C.Z., Y.Z., Z. Chen, Q.Q., J.W., H.Z., Yangxin Chen).Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China. (M.W., W.Z., Z.Z., Q.G., Yangwei Cai, G.L., Z. Cao, C.Z., Y.Z., Z. Chen, Q.Q., J.W., H.Z., Yangxin Chen). · pubmed

Paper

Abstract

SIRT5 (sirtuin 5) is a member of the sirtuin family known to regulate cardiac metabolism, aging, and function. However, its role in cardiac fibroblast (CFB) metabolism, activation, and fibrosis remains elusive.

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Research summary

SIRT5 regulates cardiac fibroblast metabolism and fibrosis through PCK2 desuccinylation. The study addresses metabolic reprogramming in cardiac fibroblasts, which is relevant to understanding aging-related cardiac dysfunction and potential interventions.

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