Depletion of Endothelial Prolyl Hydroxylase Domain Protein 2 and 3 Promotes Cardiomyocyte Proliferation and Prevents Ventricular Failure Induced by Myocardial Infarction.

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作者： Qiying,Fan ^[1] ; Hua,Mao ^[1] ; Aude,Angelini ^[1] ; Cristian,Coarfa ^[2] ; Matthew J,Robertson ^[3] ; William R,Lagor ^[2] ; Xander H T,Wehrens ^[3] ; James F,Martin ^[4] ; Xinchun,Pi ^[1] ; Liang,Xie ^[4]

作者单位： Cardiovascular Research Institute, Department of Medicine (Q.F., H.M., A.A., X.H.T.W., X.P., L.X.), Baylor College of Medicine, Houston, TX. ^[1] Departments of Molecular and Cellular Biology (C.C., M.J.R.), Baylor College of Medicine, Houston, TX. ^[2] Dan L. Duncan Comprehensive Cancer Center, Center for Precision Environmental Health (C.C., M.J.R.), Baylor College of Medicine, Houston, TX. ^[3] Department of Molecular Physiology and Biophysics (W.R.L., X.H.T.W., J.F.M.), Baylor College of Medicine, Houston, TX. ^[4] Cardiovascular Research Institute, Department of Medicine (X.H.T.W.), Baylor College of Medicine, Houston, TX. ^[5] Department of Pediatrics (X.H.T.W.), Baylor College of Medicine, Houston, TX. ^[6] Center for Space Medicine (X.H.T.W.), Baylor College of Medicine, Houston, TX. ^[7] Cardiovascular Research Institute, Program in Developmental Biology (J.F.M.), Baylor College of Medicine, Houston, TX. ^[8] The Texas Heart Institute, Houston (J.F.M.). ^[9]

关键词 cell proliferation endothelial cells heart failure hypoxia myocardial infarction myocytes, cardiac regeneration