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Oxidative Stress by Monoamine Oxidase Mediates Receptor-Independent Cardiomyocyte Apoptosis by Serotonin and Postischemic Myocardial Injury
Author(s) -
Pascale Bianchi,
Oksana Kunduzova,
Emanuela Masini,
Claudie Cambon,
Danièle Bani,
Laura Raimondi,
MarieHélène Séguélas,
Silvia Nistri,
Wilson S. Colucci,
Nathalie Leducq,
Angelo Parini
Publication year - 2005
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.104.528133
Subject(s) - oxidative stress , monoamine oxidase , pharmacology , medicine , apoptosis , monoamine oxidase a , downregulation and upregulation , serotonin , reactive oxygen species , ischemia , mitochondrion , receptor , endocrinology , microbiology and biotechnology , chemistry , biochemistry , biology , enzyme , gene
Serotonin (5-hydroxytryptamine [5-HT]), released by activated platelets during cardiac ischemia, is metabolized by the mitochondrial enzyme monoamine oxidase A (MAO-A). Because hydrogen peroxide is one of the byproducts of 5-HT degradation by MAO-A, we investigated the potential role of reactive oxygen species generated by MAOs in 5-HT-dependent cardiomyocyte death and post-ischemia-reperfusion cardiac damage.

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