长寿蛋白p66是新生儿心脏再生所必需的。

The longevity protein p66 is required for neonatal heart regeneration.

作者信息

Huang Chengzhen, Ding Tong, Zhang Yuan, Li Xunkai, Sun Xin, Lv Shuangjie, Hao Yanyan, Bai Lina, Liu Ning, Xie Yifan, Chen Houzao, Nie Yu

机构信息

State Key Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine and Peking Union Medical College, 5 Dong Dan San Tiao, Beijing 100005, PR China; State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.

State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; Department of Cardiac Surgery, Peking University Third Hospital, 49 N Garden Rd, Haidian District, Beijing 100191, PR China.

出版信息

J Mol Cell Cardiol. 2023 Apr;177:21-27. doi: 10.1016/j.yjmcc.2023.02.004. Epub 2023 Feb 22.

DOI:10.1016/j.yjmcc.2023.02.004

PMID:36827872

Abstract

The longevity protein p66 is essential for the senescence signaling that is involved in heart regeneration and remodeling. However, the exact role of p66 in heart regeneration is unknown. In this study, we found that p66 deficiency decreased neonatal mouse cardiomyocyte (CM) proliferation and impeded neonatal heart regeneration after apical resection injury. RNA sequencing and functional verification demonstrated that p66 regulated CM proliferation by activating β-catenin signaling. These findings reveal the critical role of p66 in neonatal heart regeneration and provide new insights into senescence signaling in heart regeneration.

摘要

长寿蛋白p66对于参与心脏再生和重塑的衰老信号传导至关重要。然而，p66在心脏再生中的确切作用尚不清楚。在本研究中，我们发现p66缺乏会降低新生小鼠心肌细胞（CM）的增殖，并阻碍心尖切除损伤后的新生心脏再生。RNA测序和功能验证表明，p66通过激活β-连环蛋白信号传导来调节CM增殖。这些发现揭示了p66在新生心脏再生中的关键作用，并为心脏再生中的衰老信号传导提供了新的见解。