P53 promotes cardiac dysfunction in diabetic mellitus caused by excessive mitochondrial respiration-mediated reactive oxygen species generation and lipid accumulationlipid accumulation

Circulation: Heart Failure

Volumn 5, Issue 1, 2012, Pages 106-115

  Nakamura, Hideo ^a   Matoba, Satoaki ^a   Iwai Kanai, Eri ^a,b   Kimata, Masaki ^a   Hoshino, Atsushi ^a   Nakaoka, Mikihiko ^a   Katamura, Maki ^a   Okawa, Yoshifumi ^a   Ariyoshi, Makoto ^a   Mita, Yuichiro ^a   Ikeda, Koji ^a   Okigaki, Mitsuhiko ^a   Adachi, Souichi ^c   Tanaka, Hideo ^a   Takamatsu, Tetsuro ^a   Matsubara, Hiroaki ^a  

^a KYOTO PREFECTURAL UNIVERSITY   (Japan)

^b MEIJI UNIVERSITY OF INTEGRATIVE MEDICINE   (Japan)

^c KYOTO UNIVERSITY   (Japan)

Author keywords

Cardiomyopathy; Diabetes mellitus; Free radicals; Heart failure; Metabolism; Mitochondria

Indexed keywords

CD36 ANTIGEN; CYTOCHROME C OXIDASE; PROTEIN P53; PROTEIN SCO2; REACTIVE OXYGEN METABOLITE; UNCLASSIFIED DRUG; FATTY ACID; SCO2 PROTEIN, MOUSE; STREPTOZOCIN;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DIABETIC CARDIOMYOPATHY; DNA DAMAGE; ENERGY METABOLISM; ENZYME ACTIVITY; FATTY ACID METABOLISM; FATTY ACID TRANSPORT; HEART MUSCLE CELL; HEART PERFORMANCE; LIPID METABOLISM; LIPID STORAGE; LIPOTOXICITY; MALE; MITOCHONDRIAL RESPIRATION; MOUSE; NONHUMAN; OXYGEN CONSUMPTION; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION; STREPTOZOCIN DIABETES; UPREGULATION; ANIMAL; C57BL MOUSE; CHEMICALLY INDUCED DISORDER; DIABETES MELLITUS; DISEASE MODEL; EXPERIMENTAL DIABETES MELLITUS; GENETICS; HEART MITOCHONDRION; METABOLISM; MOUSE MUTANT; PHYSIOLOGY;

ANIMALS; ANTIGENS, CD36; DIABETES COMPLICATIONS; DIABETES MELLITUS, EXPERIMENTAL; DIABETIC CARDIOMYOPATHIES; DISEASE MODELS, ANIMAL; ELECTRON TRANSPORT COMPLEX IV; FATTY ACIDS; LIPID METABOLISM; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MICE, MUTANT STRAINS; MITOCHONDRIA, HEART; MYOCYTES, CARDIAC; OXYGEN CONSUMPTION; REACTIVE OXYGEN SPECIES; STREPTOZOCIN; TUMOR SUPPRESSOR PROTEIN P53;

EID: 84859642245     PISSN: 19413289     EISSN: 19413297     Source Type: Journal    
DOI: 10.1161/CIRCHEARTFAILURE.111.961565     Document Type: Article

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