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Uncompensated mitochondrial oxidative stress underlies heart failure in an iPSC-derived model of congenital heart disease
Institution:1. Department of Developmental Biology, University of Pittsburgh, Pittsburgh, PA, USA;2. Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA;3. Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA;4. Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, USA;5. Department of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA, USA;6. Department of Computational & Systems Biology and Pittsburgh Center for Evolutionary Biology and Medicine, University of Pittsburgh, Pittsburgh, PA, USA;7. Anesthesiology, University of Pittsburgh, Pittsburgh, PA, USA;8. Division of Biomedical Informatics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA;9. Department of Electrical Engineering and Computer Science, University of Cincinnati, Cincinnati, OH, USA;10. Department of Biomedical Informatics, University of Cincinnati, Cincinnati, OH, USA;11. Department of Pediatrics, University of Cincinnati School of Medicine, Cincinnati, OH 45256, USA;12. Fischell Department of Bioengineering, University of Maryland, College Park, MD, USA;13. Centre for Cardiovascular Genomics and Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China;14. Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA;15. Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA;16. Departments of Pediatrics and Environmental Medicine University of Rochester Medical Center Rochester, NY USA;17. Pediatrics, Pharmacology, and Physiology, Aab Cardiovascular Research Institute, University of Rochester Medical Center, Rochester, NY, USA;18. Supercomputer Education and Research Centre, Indian Institute of Science, Bangalore, India
Abstract:
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  • Keywords:heart failure  hypoplastic left heart syndrome  congenital heart disease  induced pluripotent stem-cell-derived cardiomyocytes  i  mitochondrial permeability transition pore  endoplasmic reticulum stress  oxidative stress  antioxidant response  sildenafil  TUDCA
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