TL;DR
It is suggested that ERK5-Cyclin D1 signaling contributes to the hypertrophic phenotype of RAF1-mutant cardiomyocytes and support further investigation of BBR as a potential therapeutic candidate for RAF1-associated NS-HCM.
Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) provide a scalable platform for cardiovascular research but remain structurally and functionally immature, limiting their utility for studying cardiac biology, disease mechanisms, and clinical translation. Developmental signaling pathways that coord...
EHTs generated from HCM hiPSC-derived cardiomyocytes showed a progressive decline in apparent force, whereas DCM EHTs fractured over time, suggesting mutation-associated phenotypes in 3D cardiac tissue models, and highlight the utility of hiPSC-based cardiac models for investigating molecular and functional disease mec...
BACKGROUND In heart failure (HF), DNA damage caused by various external stressors contributes to cardiac dysfunction through the activation of DNA damage response pathways. To date, no clinical strategies have been established to restore cardiac function by reducing accumulated DNA damage. We previously found that vita...
It is demonstrated that loss of Smyd5 induces rapid progression to heart failure accompanied by robust inflammatory activation, including a ∼100-fold increase in Il-6 expression, accompanied by rapid progression of cardiac remodeling and heart failure.
Background Zebrafish regenerate their hearts after injury, and defining the barriers that block this capacity in mammals may reveal targets for heart failure treatment. Elevated levels of the cardiomyocyte-specific kinase TNNI3K are associated with human cardiomyopathy, and its overexpression drives adverse remodeling...
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