The longevity protein p66Shc is required for neonatal heart regeneration

In this study, we found that p66Shc deficiency decreased neonatal mouse cardiomyocyte (CM) proliferation and impeded neonatal heart regeneration after apical resection injury. RNA sequencing and functional verification demonstrated that p66Shc regulated CM proliferation by activating β-catenin signaling. These findings reveal the critical role of p66Shc in neonatal heart regeneration and provide new insights into senescence signaling in heart regeneration.

Source: Journal of Molecular and Cellular Cardiology - February 22, 2023 Category: Cytology Authors: Chengzhen Huang, Tong Ding, Yuan Zhang, Xunkai Li, Xin Sun, Shuangjie Lv, Yanyan Hao, Lina Bai, Ning Liu, Yifan Xie, Houzao Chen, Yu Nie Source Type: research