ArticleMolecular medicine reports2025
HIF‑1α overexpression improves the efficacy of human induced pluripotent stem cell‑derived cardiomyocytes for cardiac repair following myocardial infarction.
Article in Molecular medicine reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- MITF Regulates CFTR Expression to Participate in Myocardial Ischemia-Reperfusion Injury.The journal of gene medicine · 2026Article
- Towards human cardiac new approach methodologies (NAMs) to evaluate the combination of repolarization prolonging and shortening drugs: a pilot study.Frontiers in drug discovery · 2025Article
- Hypoxia and Tissue Regeneration: Adaptive Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Glycometabolic Regulation of Angiogenesis: Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2025Review
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Authors and funding
3 authors.
Funding
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Abstract
Myocardial infarction (MI) is the leading cause of death worldwide and currently there are limited therapies that can regenerate the lost cardiac cells following MI. To enhance the therapeutic effects of human induced pluripotent stem cell‑derived cardiomyocytes (hiPSC‑CM) transplantation for treatment of MI, the present study sought to increase the pro‑angiogenic effect of hiPSC‑CM by overexpressing a mutated hypoxia‑inducible factor 1‑alpha (HIF‑1α; P402A; P564A) via lentivirus transfection. Morphology and the electrophysiology of the genetically engineered cell were both unchanged. The present study demonstrated that the proangiogenic factors in the conditioned medium of the HIF‑1α‑overexpressing hiPSC‑CM (HIF‑CM) were upregulated and subsequently resulted to the rescue of the tube forming ability and migratory ability of the hypoxia‑injured human umbilical vein endothelial cells. Using a MI mouse model, the present study demonstrated that the transplantation of HIF‑CM greatly improved cardiac function, decreased scar size, promoted the concentration of the proangiogenic factors in circulation and promoted the neovessel formation in mice with MI. In conclusion, HIF‑1α‑overexpressing hiPSC‑CM could increase the angiogenesis of endothelial cells and mediate cardioprotection in mouse following MI.
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