Front Biosci (Landmark Ed). 2025 Jul 30;30(7):39676. doi: 10.31083/FBL39676.
ABSTRACT
BACKGROUND: Heart regeneration requires renewal of lost cardiomyocytes. However, the mammalian heart loses its proliferative capacity soon after birth, and the molecular signaling underlying the loss of cardiac proliferation postnatally is not fully understood.
PURPOSE: This study aimed to investigate the role of Catenin alpha 3 (Ctnna3), coding for alpha T catenin (αT-catenin) protein in regulating cardiomyocyte proliferation and heart regeneration during the neonatal period.
METHODS: Here we report that ablation of Ctnna3 and highly expressed in hearts, accelerated heart regeneration following heart apex resection in neonatal mice.
RESULTS: Our results show that Ctnna3 deficiency enhances cardiomyocyte proliferation in hearts from postnatal day 7 (P7) mice by upregulating Yes-associated protein (Yap) expression.
CONCLUSION: Our study demonstrates that Ctnna3 deficiency is sufficient to promote heart regeneration and cardiomyocyte proliferation in neonatal mice and indicates that functional interference of α-catenins might help to stimulate myocardial regeneration after injury.
PMID:40765350 | DOI:10.31083/FBL39676
