The overexpression of Twinkle helicase ameliorates the progression of cardiac fibrosis and heart failure in pressure overload model in mice

Myocardial mitochondrial DNA (mtDNA) copy number decreases in heart failure. In post-myocardial infarction mice, increasing mtDNA copy number by overexpressing mitochondrial transcription factor attenuates mtDNA deficiency and ameliorates pathological remodeling thereby markedly improving survival....

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Veröffentlicht in:	PloS one 2013-06, Vol.8 (6), p.e67642-e67642
Hauptverfasser:	Tanaka, Atsushi, Ide, Tomomi, Fujino, Takeo, Onitsuka, Ken, Ikeda, Masataka, Takehara, Takako, Hata, Yuko, Ylikallio, Emil, Tyynismaa, Henna, Suomalainen, Anu, Sunagawa, Kenji
Format:	Artikel
Sprache:	eng
Schlagworte:	Angiotensin Angiotensin II Animals Aorta Aorta - pathology Biology Biosynthesis Blood pressure Cardiovascular disease Cardiovascular diseases Collagen Connective tissue growth factor Connective tissues Constriction Copy number Coronary artery disease Deoxyribonucleic acid Diastolic pressure Disease Models, Animal Disease Progression DNA DNA Copy Number Variations - genetics DNA helicase DNA Helicases - genetics Echocardiography Echocardiography - methods Fibroblasts Fibrosis Fibrosis - genetics Fibrosis - pathology Gene Expression - genetics Heart Heart attacks Heart diseases Heart failure Heart Failure - genetics Heart Failure - pathology Hypertension Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - pathology Laboratory animals Male Mathematics Medical research Medicine Mice Mice, Transgenic - genetics Mitochondrial DNA Mitochondrial Proteins - genetics Mutation Myocardial infarction Neurology Pressure Proteins Rodents Studies Transcription factors Transforming growth factor Transgenic animals Transgenic mice Ventricle Ventricular Function, Left - genetics Ventricular Remodeling - genetics Wall thickness
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