Major Contribution of the 3/6/7 Class of TRPC Channels to Myocardial Ischemia/Reperfusion and Cellular Hypoxia/Reoxygenation Injuries
Major contribution of the 3/6/7 class of TRPC channels to myocardial ischemia/reperfusion and cellular hypoxia/reoxygenation injuries Xiju Hea,b,c,1, Shoutian Lia,b,1, Benju Liua,b, Sebastian Susperreguyd, Karina Formosod, Jinghong Yaoe, Jinsong Kangf, Anbing Shig, Lutz Birnbaumerd,h,2, and Yanhong Liaoa,b,i,2 aDepartment of Anatomy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China; bInstitute of Brain Research, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China; cDepartment of Anatomy, Hubei University of Medicine, Shiyan, 442000, China; dInstitute of Biomedical Research (BIOMED), Catholic University of Argentina, Buenos Aires C1107AFF, Argentina; eDepartment of Infectious Disease, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China; fDepartment of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China; gDepartment of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China; hNeurobiology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709; and iKey Laboratory of Neurological Diseases of Ministry of Education, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China Contributed by Lutz Birnbaumer, February 24, 2017 (sent for review December 28, 2016; reviewed by Thomas Gudermann and Eric N. Olson) The injury phase after myocardial infarcts occurs during reperfusion of the mitochondrial permeability transition pore (mPTP) (2). Im- and is a consequence of calcium release from internal stores mediately after mPTP activation, mitochondria swell and release combined with calcium entry, leading to cell death by apoptopic apoptogenic and necrogenic factors, which activate caspase-dependent and necrotic processes.
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