Language
English
Publication Date
1-23-2026
Journal
Life Science Alliance
DOI
10.26508/lsa.202503496
PMID
41577381
PMCID
PMC12830084
PubMedCentral® Posted Date
1-23-2026
PubMedCentral® Full Text Version
Post-print
Abstract
Adult mammalian hearts exhibit limited regenerative capacity because of the restricted renewal of cardiomyocytes. Recent studies reveal that mammalian hearts exhibit transient regenerative potential within a short time frame after birth, suggesting a regulatory mechanism that prevents adult hearts from initiating a regenerative response to cardiac injury. Here, we discovered that an active form of YAP, named YAP6SA, which is not inhibited by the Hippo signaling pathway and does not interact with TEADs, induces cardiomyocyte cell cycle reentry. In addition, YAP6SA interacts with scaffold protein MPDZ to regulate Rho GTPases and promote cell cycle progression in cardiomyocytes (CMs). Importantly, YAP6SA overexpression is well tolerated in mammalian hearts. These findings provide new insights into YAP function in cardiomyocytes.
Keywords
Myocytes, Cardiac, Animals, Cell Cycle, YAP-Signaling Proteins, Mice, Signal Transduction, Adaptor Proteins, Signal Transducing, Transcription Factors, Cell Cycle Proteins, Humans, rho GTP-Binding Proteins, DNA-Binding Proteins, Hippo Signaling Pathway, Phosphoproteins, Regeneration, TEA Domain Transcription Factors
Published Open-Access
yes
Recommended Citation
Xie, Bing; Steimle, Jeffrey; Deshmukh, Vaibhav; et al., "TEAD-Independent Mechanisms of YAP Function in Cardiomyocyte Cell Cycle Reentry" (2026). Faculty, Staff and Students Publications. 3433.
https://digitalcommons.library.tmc.edu/baylor_docs/3433
Included in
Biochemical Phenomena, Metabolism, and Nutrition Commons, Biomedical Informatics Commons, Diseases Commons, Neurology Commons, Neurosciences Commons, Pediatrics Commons