M
Michael Kinter
Researcher at Oklahoma Medical Research Foundation
Publications - 135
Citations - 7847
Michael Kinter is an academic researcher from Oklahoma Medical Research Foundation. The author has contributed to research in topics: Oxidative stress & Mitochondrion. The author has an hindex of 43, co-authored 121 publications receiving 6568 citations. Previous affiliations of Michael Kinter include Central South University & Cleveland Clinic Lerner Research Institute.
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Journal ArticleDOI
Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease
Lemin Zheng,Benedicta Nagella Nukuna,Marie Luise Brennan,Mingjiang Sun,Marlene Goormastic,Megan Settle,Dave Schmitt,Xiaoming Fu,Leonor Thomson,Paul L. Fox,Harry Ischiropoulos,Jonathan D. Smith,Michael Kinter,Stanley L. Hazen +13 more
TL;DR: The present results provide the first direct evidence for apoA-I as a selective target forMPO-catalyzed oxidative modification in human atheroma and suggest a potential mechanism for MPO-dependent generation of a proatherogenic dysfunctional form of HDL in vivo.
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The oxygen-rich postnatal environment induces cardiomyocyte cell-cycle arrest through DNA damage response.
Bao N. Puente,Wataru Kimura,Shalini Muralidhar,Jesung Moon,James F. Amatruda,Katherine J Phelps,David Grinsfelder,Beverly A. Rothermel,Rui Chen,Joseph A. Garcia,Celio X.C. Santos,Suwannee Thet,Eiichiro Mori,Michael Kinter,Paul M. Rindler,Serena Zacchigna,Shibani Mukherjee,David J. Chen,Ahmed I. Mahmoud,Mauro Giacca,Peter S. Rabinovitch,Asaithamby Aroumougame,Ajay M. Shah,Luke I. Szweda,Hesham A. Sadek +24 more
TL;DR: It is shown that reactive oxygen species (ROS), oxidative DNA damage, and DNA damage response (DDR) markers significantly increase in the heart during the first postnatal week, revealing a protective mechanism that mediates cardiomyocyte cell-cycle arrest in exchange for utilization of oxygen-dependent aerobic metabolism.
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Hypoxia induces heart regeneration in adult mice
Yuji Nakada,Diana C. Canseco,Suwannee Thet,Salim Abdisalaam,Aroumougame Asaithamby,Celio X.C. Santos,Ajay M. Shah,Hua Zhang,James E. Faber,Michael Kinter,Luke I. Szweda,Chao Xing,Zeping Hu,Ralph J. DeBerardinis,Gabriele G. Schiattarella,Joseph A. Hill,Orhan K. Öz,Zhigang Lu,Cheng Cheng Zhang,Wataru Kimura,Wataru Kimura,Hesham A. Sadek +21 more
TL;DR: It is demonstrated that the endogenous regenerative properties of the adult mammalian heart can be reactivated by exposure to gradual systemic hypoxaemia, and the potential therapeutic role of hypoxia in regenerative medicine is highlighted.
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Polycystin-1, STAT6, and P100 function in a pathway that transduces ciliary mechanosensation and is activated in polycystic kidney disease.
Seng Hui Low,Shivakumar Vasanth,Shivakumar Vasanth,Claire H. Larson,Sambuddho Mukherjee,Nikunj Sharma,Nikunj Sharma,Michael Kinter,Michelle E. Kane,Tomoko Obara,Thomas Weimbs +10 more
TL;DR: It is shown that PC1 undergoes proteolytic cleavage that results in nuclear translocation of its cytoplasmic tail and that this pathway is inappropriately activated in ADPKD.
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Glycation of mitochondrial proteins from diabetic rat kidney is associated with excess superoxide formation
Mariana G. Rosca,Tiberiu G. Mustata,Michael Kinter,Aylin M. Ozdemir,Timothy S. Kern,Luke I. Szweda,Michael Brownlee,Vincent M. Monnier,Miriam F. Weiss +8 more
TL;DR: Posttranslational modifications of mitochondrial proteins by MGO may represent pathogenic events leading to mitochondria-induced oxidative stress in the kidney in chronic diabetes.