Open AccessSuper-Suppression of Mitochondrial Reactive Oxygen Species Signaling Impairs Compensatory Autophagy in Primary Mitophagic Cardiomyopathy
Author(s) -
Moshi Song,
Yun Chen,
Guohua Gong,
Elizabeth Murphy,
Peter S. Rabinovitch,
Gerald W. Dorn
Publication year - 2014
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.115.304384
Subject(s) - reactive oxygen species , autophagy , mitochondrion , microbiology and biotechnology , cardiomyopathy , mitochondrial dna , biology , primary (astronomy) , mitophagy , signal transduction , chemistry , apoptosis , medicine , biochemistry , heart failure , gene , physics , astronomy
Mitochondrial reactive oxygen species (ROS) are implicated in aging, chronic degenerative neurological syndromes, and myopathies. On the basis of free radical hypothesis, dietary, pharmacological, and genetic ROS suppression has been tested to minimize tissue damage, with remarkable therapeutic efficacy. The effects of mitochondrial-specific ROS suppression in primary mitophagic dysfunction are unknown.
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