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NecroX-5 prevents hypoxia/reoxygenation injury by inhibiting the mitochondrial calcium uniporter
Author(s) -
Vũ Thị Thu,
Hyoung Kyu Kim,
Lê Thành Long,
Sungryul Lee,
Tran My Hanh,
Tae Hee Ko,
Hye-Jin Heo,
Nari Kim,
Soon Ha Kim,
Kyung Soo Ko,
Byoung Doo Rhee,
Jin Han
Publication year - 2012
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvs122
Subject(s) - uniporter , mitochondrion , mitochondrial permeability transition pore , hypoxia (environmental) , pharmacology , oxidative stress , ischemia , calcium , ouabain , inner mitochondrial membrane , reactive oxygen species , chemistry , microbiology and biotechnology , medicine , biology , endocrinology , oxygen , biochemistry , cytosol , programmed cell death , apoptosis , organic chemistry , enzyme , sodium
Preservation of mitochondrial function is essential to limit myocardial damage in ischaemic heart disease. We examined the protective effects and mechanism of a new compound, NecroX-5, on rat heart mitochondria in a hypoxia/reoxygenation (HR) model.

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