FHOD3 deficiency disrupts sarcomere organization and activates caMKII signaling in human stem cell-derived cardiomyocytes
Summary
Our study establishes a valuable human-derived model for investigating the molecular mechanisms of FHOD3 deficiency-induced cardiomyopathy. This model allows for extensive investigation into the phenotypes caused by FHOD3 deficiency and identifies CaMKII activation as a crucial factor contributing to the HF phenotype. Additionally, this model serves as an important tool for discovering novel therapeutic agents, and we demonstrate that OM can partially improve myocardial function in FHOD3 KO hESC-CMs. © 2026. The Author(s).
| Authors | Wei M, Hou X, Zhang S, Hu X, Chen X, Gao Z, Xu S, Shi Z, Zhu M, Lan F, Cui M |
|---|---|
| Journal | Stem cell research & therapy |
| Publication Date | 2026 Jan 16;17(1):82 |
| PubMed | 41540467 |
| PubMed Central | PMC12892442 |
| DOI | 10.1186/s13287-026-04902-z |