Open AccessResponse to Letter Regarding Article, “Mitochondrial DNA Damage Can Promote Atherosclerosis Independently of Reactive Oxygen Species Through Effects on Smooth Muscle Cells and Monocytes and Correlates With Higher-Risk Plaques in Humans”
Author(s) -
Emma Yu,
Patrick A. Calvert,
John R. Mercer,
J. B. Harrison,
Lauren Baker,
Nichola Figg,
Sheetal Kumar,
Julie J. Wang,
Liam A. Hurst,
Daniel R. Obaid,
Angela Logan,
Nick E.J. West,
Murray C.H. Clarke,
António Vidal-Puig,
Michael P. Murphy,
Martin R. Bennett
Publication year - 2014
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.113.008032
Subject(s) - medicine , reactive oxygen species , mitochondrial dna , monocyte , pathology , immunology , microbiology and biotechnology , biochemistry , gene , biology
We welcome the opportunity to respond to comments from Drs Stocker and Maghzal on our article.1 Increased reactive oxygen species (ROS) occur in human atherosclerosis in many cell types, and multiple experimental manipulations (predominantly in mice) suggest that ROS promote atherosclerosis. Because mitochondria are an important source of ROS that could be amplified by mitochondrial DNA (mtDNA) damage, the concept has arisen that mtDNA damage promotes atherosclerosis by elevating ROS. However, the polymerase-γ proofreading activity (polG) mouse model of mtDNA damage has been extensively characterized using multiple methods and does not show increased ROS by the age atherosclerosis was studied. Our use of the mitochondria-targeted mass spectrometry probe MitoB (Figure 2C) supported this interpretation. We also showed no difference in …
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