The longevity protein p66Shc is required for neonatal heart regeneration

The longevity protein p66Shc is essential for the senescence signaling that is involved in heart regeneration and remodeling. However, the exact role of p66Shc in heart regeneration is unknown. 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 beta-catenin signaling. These findings reveal the critical role of p66Shc in neonatal heart regeneration and provide new insights into senescence signaling in heart regeneration.

Automated summary

The protein p66Shc plays a crucial role in heart regeneration by promoting neonatal mouse cardiomyocyte proliferation and facilitating heart regeneration. The study also reveals that p66Shc regulates cardiomyocyte proliferation through the activation of beta-catenin signaling. These findings provide new insights into senescence signaling in heart regeneration.