ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
KLF1 Promotes Cardiomyocyte Proliferation and Heart Regeneration Through Regulation of Wnt/β-Catenin Signaling Pathway.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- DMBT1 in Adipose-Derived Stem Cell-Derived Exosomes Participates in Alleviating Ferroptosis to Promote Diabetic Wound Healing.Stem cell reviews and reports · 2026Article
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
- Cardiac regeneration and repair: the emerging mechanisms and therapeutic approaches.Molecular biomedicine · 2026Review
- Review
- Paligenosis: dual potential of mature cell plasticity in regeneration and tumorigenesis.MedScience · 2026Review
- Global Evaluation of Congenital Heart Disease-Associated Non-Coding Variants.Research square · 2026Article
- Cardiomyocyte-derived BDNF restricts cardiac fibrosis by decreasing the activity of the TGF-β/Smad2/3 pathway and increasing Smad7 expression.Frontiers in cell and developmental biology · 2026Article
- c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026Review
- NR4A1 Regulates Glycolysis in M1 Macrophages via the Wnt/β-Catenin Pathway to Affect Sepsis-Induced Myocardial Injury.Journal of inflammation research · 2026Article
- Article
- Acute Myocardial Infarction: Molecular Pathogenesis, Diagnosis, and Clinical Management.MedComm · 2025Review
- KLF1 Promotes Cardiomyocyte Proliferation and Heart Regeneration Through Regulation of Wnt/β-Catenin Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Innovative therapeutic approaches for heart failure, a leading cause of mortality worldwide, are urgently needed. In this study, the important role of Krüppel-like factor 1 (KLF1) in cardiomyocyte proliferation and heart regeneration is explored, and revealed its ability to regulate the Wnt/β-catenin signaling pathway as well as exploring a feasible strategy to target KLF1 for the treatment of heart failure. Postnatally, a marked decrease in KLF1 expression occurred almost simultaneously with a reduction in myocardial regenerative capacity. Through comprehensive in vivo and in vitro studies, it is demonstrated that in neonatal and adult mice, KLF1 overexpression significantly increased cardiomyocyte proliferation and promoted myocardial repair following infarction, whereas KLF1 knockout abolished these effects. Mechanistically, through RNA sequencing (RNA-seq) and ATAC sequencing (ATAC-seq) analyses, it is revealed that the promotion of cardiomyocyte proliferation by KLF1 is associated with the Wnt/β-catenin signaling pathway, mitochondrial function, and fatty acid metabolism. These findings highlight the important role of KLF1 in cardiomyocyte proliferation and heart regeneration, which provides novel insights into therapeutic targets for heart failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.