Key result
Cardiomyocyte YAP represses MEF2 pathways to curb AngII-induced inflammation and fibrosis.
Why the study?
YAP's role in cardiomyocytes in repressing myocardial inflammation and fibrosis and regulating MEF2-dependent pathways under stress was not fully understood.
Cardiomyocyte YAP protects against maladaptive inflammation and fibrosis during AngII stress by repressing MEF2-dependent pathways.
YAP is increasingly recognized for its role in safeguarding the heart by regulating cardiac responses to mechanical and ischemic stress. Here, we highlight YAP's protective role in cardiomyocytes by restraining maladaptive inflammation and fibrosis in response to AngII stress. By selective deletion of cardiomyocyte YAP and single-nuclei RNA sequencing, we determine that YAP serves an anti-inflammatory role and suggest that this occurs through repression of MEF2-dependent pathways, advancing our understanding of how YAP functions in cardiac health and disease.
No takes yet. Share an insight, caveat, or question.
Ninh et al. (2025) studied Myocardial inflammation and fibrosis in response to AngII stress. Selective deletion of cardiomyocyte YAP was evaluated on Inflammation, fibrosis, and MEF2-dependent pathway expression. Selective deletion of cardiomyocyte YAP revealed that YAP serves an anti-inflammatory role by repressing MEF2-dependent pathways in response to AngII stress.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: