Ctnna3 Deficiency Promotes Heart Regeneration by Enhancing Cardiomyocyte Proliferation in Neonatal Mice.

IF 3.1 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Frontiers in bioscience (Landmark edition) Pub Date : 2025-07-30 DOI:10.31083/FBL39676

Sha Zou, Wuhou Dai, Wufan Tao, Jifen Li, Zeyi Cheng, Hongyan Wang

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引用次数: 0

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.

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Ctnna3缺乏通过增强新生小鼠心肌细胞增殖促进心脏再生。

背景：心脏再生需要丢失的心肌细胞的更新。然而，哺乳动物的心脏在出生后不久就失去了它的增殖能力，并且在出生后心脏增殖丧失的分子信号还不完全清楚。目的：本研究旨在探讨编码αT Catenin （αT-catenin）蛋白的Catenin α 3 （Ctnna3）在新生儿期心肌细胞增殖和心脏再生中的作用。方法：我们在此报道了Ctnna3在心脏中高表达的消融，加速了新生小鼠心尖切除后的心脏再生。结果：我们的研究结果表明，Ctnna3缺乏通过上调yes相关蛋白（Yap）的表达来增强出生后第7天（P7）小鼠心脏的心肌细胞增殖。结论：本研究表明，Ctnna3缺乏足以促进新生小鼠心脏再生和心肌细胞增殖，α-连环蛋白的功能干扰可能有助于刺激损伤后心肌再生。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in bioscience (Landmark edition)

CiteScore

3.50

自引率

0.00%

发文量