ArticleScientific reports2021
Human induced pluripotent stem cell-based platform for modeling cardiac ischemia.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Multi-Omics Integration Reveals Incomplete Reactivation of Developmental Cell-Cycle Programs in Adult Human Infarcted Hearts.Chemical biology & drug design · 2026Article
- Vascularized Cardiac Tissue Engineering: From Advances in Biofabrication to Translational Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Humanized hiPSC Platforms for I/R Injury: Advancing Toward Precision Cardioprotection.Cardiovascular therapeutics · 2026Review
- Maturation is required to model ischemia-reperfusion injury in engineered human cardiac tissues.Frontiers in bioengineering and biotechnology · 2026Article
- Imaging Oxygen Concentrations in Bone Scaffolds during Cellular Activity and Fluid Perfusion.ACS biomaterials science & engineering · 2025Article
- Cardiac Tissue Engineering for Translational Cardiology: From In Vitro Models to Regenerative Therapies.Bioengineering (Basel, Switzerland) · 2025Review
- Mitophagy is induced in human engineered heart tissue after simulated ischemia and reperfusion.Journal of cell science · 2025Article
- Cardioprotection by poloxamer 188 is mediated through increased endothelial nitric oxide production.Scientific reports · 2025Article
- Inhibition of ceramide synthesis improves the outcome of ischemia/reperfusion injury in cardiomyocytes derived from human induced pluripotent stem cell.Stem cell research & therapy · 2025Article
- Modelling myocardial ischemia/reperfusion injury with inflammatory response in human ventricular cardiac organoids.Cell proliferation · 2025Article
- A hypoxia-on-a-chip platform for modeling ischemic arrhythmogenesis and evaluating the effects of levosimendan and OR-1896 on ischemic human iPSC-derived cardiomyocytes.Frontiers in bioengineering and biotechnology · 2025Article
- The Current State of Realistic Heart Models for Disease Modelling and Cardiotoxicity.International journal of molecular sciences · 2024Review
- miR-124-3p downregulates EGR1 to suppress ischemia-hypoxia reperfusion injury in human iPS cell-derived cardiomyocytes.Scientific reports · 2024Article
- Hypoxia and re-oxygenation effects on human cardiomyocytes cultured on polycaprolactone and polyurethane nanofibrous mats.Journal of biological engineering · 2024Article
- In vivo phage display identifies novel peptides for cardiac targeting.Scientific reports · 2024Article
- In silico study of the mechanisms of hypoxia and contractile dysfunction during ischemia and reperfusion of hiPSC cardiomyocytes.Disease models & mechanisms · 2024Article
- Multicellular 3D models to study myocardial ischemia-reperfusion injury.Frontiers in cell and developmental biology · 2024Review
- Mature human induced pluripotent stem cell-derived cardiomyocytes promote angiogenesis through alpha-B crystallin.Stem cell research & therapy · 2023Article
- Optical Mapping of Cardiomyocytes in Monolayer Derived from Induced Pluripotent Stem Cells.Cells · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic heart disease is a major cause of death worldwide, and the only available therapy to salvage the tissue is reperfusion, which can initially cause further damage. Many therapeutics that have been promising in animal models have failed in human trials. Thus, functional human based cardiac ischemia models are required. In this study, a human induced pluripotent stem cell derived-cardiomyocyte (hiPSC-CM)-based platform for modeling ischemia-reperfusion was developed utilizing a system enabling precise control over oxygen concentration and real-time monitoring of the oxygen dynamics as well as iPS-CM functionality. In addition, morphology and expression of hypoxia-related genes and proteins were evaluated as hiPSC-CM response to 8 or 24 h hypoxia and 24 h reoxygenation. During hypoxia, initial decrease in hiPSC-CM beating frequency was observed, after which the CMs adapted to the conditions and the beating frequency gradually increased already before reoxygenation. During reoxygenation, the beating frequency typically first surpassed the baseline before settling down to the values close the baseline. Furthermore, slowing on the field potential propagation throughout the hiPSC-CM sheet as well as increase in depolarization time and decrease in overall field potential duration were observed during hypoxia. These changes were reversed during reoxygenation. Disorganization of sarcomere structures was observed after hypoxia and reoxygenation, supported by decrease in the expression of sarcomeric proteins. Furthermore, increase in the expression of gene encoding glucose transporter 1 was observed. These findings indicate, that despite their immature phenotype, hiPSC-CMs can be utilized in modeling ischemia-reperfusion injury.
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