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Overexpression of Catalase Targeted to Mitochondria Attenuates Murine Cardiac Aging
Author(s) -
DaoFu Dai,
Luis F. Santana,
Marc Vermulst,
Daniela M. Tomazela,
Mary J. Emond,
Michael J. MacCoss,
Katherine A. Gollahon,
George M. Martin,
Lawrence A. Loeb,
Warren Ladiges,
Peter S. Rabinovitch
Publication year - 2009
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.108.822403
Subject(s) - reactive oxygen species , medicine , mitochondrion , mitochondrial biogenesis , catalase , cardiac function curve , mitochondrial ros , oxidative stress , senescence , endocrinology , mitochondrial dna , cardiology , biology , heart failure , microbiology and biotechnology , biochemistry , gene
Age is a major risk for cardiovascular diseases. Although mitochondrial reactive oxygen species have been proposed as one of the causes of aging, their role in cardiac aging remains unclear. We have previously shown that overexpression of catalase targeted to mitochondria (mCAT) prolongs murine median lifespan by 17% to 21%.

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