Transplantation of human iPSC-derived cardiomyocyte patches after myocardial infarction improves tissue elasticity and reduces remote fibrosis by secreting TGF-β1 to induce collagen type I production.
Does transplantation of hiPSC-derived CM patches improve tissue elasticity and reduce fibrosis in a myocardial infarction model?
hiPSC-derived cardiomyocyte patches improve cardiac elasticity and reduce fibrosis after myocardial infarction by secreting TGF-β1 to modulate fibroblast collagen production.
Myocardial infarction (MI) followed by chronic heart failure is the main cause of mortality of heart diseases. Although reparative cell transplantation therapies with pluripotent stem cell-derived cardiomyocytes (CMs) represent a promising therapeutic strategy, molecular mechanisms of the therapy remain elusive. Here, we show that transplantation of the human induced pluripotent stem cell (hiPSC)-derived CM patch onto the damaged heart after MI increases the ratio of collagen type I against collagen type III to modulate alignment of the collagen fibers at the infarcted zone. As a result, tissue elasticity of the heart is improved, and fibrosis at the remote zone is reduced. Mechanistically, we find that hiPSC-derived CM patches secrete TGF-β1, directly inducing collagen type I production in fibroblasts but not collagen type III. Our results suggest the direct effect of the transplanted CM patch on the cardiac fibroblasts to improve elasticity of the damaged heart, resulting in functional recovery after MI.
Torigata et al. (Wed,) conducted a other in Myocardial infarction. human induced pluripotent stem cell (hiPSC)-derived cardiomyocyte patch was evaluated on collagen type I to type III ratio, tissue elasticity, and fibrosis. Transplantation of human iPSC-derived cardiomyocyte patches after myocardial infarction improves tissue elasticity and reduces remote fibrosis by secreting TGF-β1 to induce collagen type I production.