KLF1 Promotes Cardiomyocyte Proliferation and Heart Regeneration Through Regulation of Wnt/β‐Catenin Signaling Pathway DOI Creative Commons

Yanglin Hao,

Feng Zhang, Shuan Ran

и другие.

Advanced Science, Год журнала: 2025, Номер unknown

Опубликована: Март 27, 2025

Innovative therapeutic approaches for heart failure, a leading cause of mortality worldwide, are urgently needed. In this study, the important role Krüppel-like factor 1 (KLF1) in cardiomyocyte proliferation and regeneration is explored, revealed its ability to regulate Wnt/β-catenin signaling pathway as well exploring feasible strategy target KLF1 treatment failure. Postnatally, marked decrease expression occurred almost simultaneously with reduction myocardial regenerative capacity. Through comprehensive vivo vitro studies, it demonstrated that neonatal adult mice, overexpression significantly increased promoted repair following infarction, whereas knockout abolished these effects. Mechanistically, through RNA sequencing (RNA-seq) ATAC (ATAC-seq) analyses, promotion by associated pathway, mitochondrial function, fatty acid metabolism. These findings highlight regeneration, which provides novel insights into targets

Язык: Английский

KLF1 Promotes Cardiomyocyte Proliferation and Heart Regeneration Through Regulation of Wnt/β‐Catenin Signaling Pathway DOI Creative Commons

Yanglin Hao,

Feng Zhang, Shuan Ran

и другие.

Advanced Science, Год журнала: 2025, Номер unknown

Опубликована: Март 27, 2025

Innovative therapeutic approaches for heart failure, a leading cause of mortality worldwide, are urgently needed. In this study, the important role Krüppel-like factor 1 (KLF1) in cardiomyocyte proliferation and regeneration is explored, revealed its ability to regulate Wnt/β-catenin signaling pathway as well exploring feasible strategy target KLF1 treatment failure. Postnatally, marked decrease expression occurred almost simultaneously with reduction myocardial regenerative capacity. Through comprehensive vivo vitro studies, it demonstrated that neonatal adult mice, overexpression significantly increased promoted repair following infarction, whereas knockout abolished these effects. Mechanistically, through RNA sequencing (RNA-seq) ATAC (ATAC-seq) analyses, promotion by associated pathway, mitochondrial function, fatty acid metabolism. These findings highlight regeneration, which provides novel insights into targets

Язык: Английский

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