Journal
CARDIOVASCULAR RESEARCH
Volume 94, Issue 2, Pages 342-350Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvs122
Keywords
NecroX-5; Mitochondria; Hypoxia; reoxygenation; Calcium uniporter
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Funding
- Priority Research Centers
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [ROA-2007-000-20085, 2010-0020224]
- National Research Foundation of Korea [2007-0056874] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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. NecroX-5 reduced mitochondrial oxidative stress, prevented the collapse in mitochondrial membrane potential, improved mitochondrial oxygen consumption, and suppressed mitochondrial Ca-2 overload during reoxygenation in an in vitro rat heart HR model. Furthermore, NecroX-5 reduced the ouabain- or histamine-induced increase in mitochondrial Ca-2. These findings suggest that NecroX-5 may act as a mitochondrial Ca-2 uniporter inhibitor to protect cardiac mitochondria against HR damage.
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