FGF21 attenuates pathological myocardial remodeling following myocardial infarction through the adiponectin-dependent mechanism

Biochemical and Biophysical Research Communications

Volumn 459, Issue 1, 2015, Pages 124-130

  Joki, Yusuke ^a,b   Ohashi, Koji ^a   Yuasa, Daisuke ^a   Shibata, Rei ^a   Ito, Masanori ^a   Matsuo, Kazuhiro ^a   Kambara, Takahiro ^a   Uemura, Yusuke ^a   Hayakawa, Satoko ^a   Hiramatsu Ito, Mizuho ^a   Kanemura, Noriyoshi ^a   Ogawa, Hayato ^a   Daida, Hiroyuki ^b   Murohara, Toyoaki ^a   Ouchi, Noriyuki ^a  

^a NAGOYA UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

^b JUNTENDO UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

Adiponectin; Cardiac remodeling; FGF21; Myocardial infarction; Myokine

Indexed keywords

ADENOVIRUS VECTOR; ADIPOCYTOKINE; ADIPONECTIN; BETA GALACTOSIDASE; CYTOKINE; FIBROBLAST GROWTH FACTOR 21; ADIPOQ PROTEIN, MOUSE; FIBROBLAST GROWTH FACTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIINFLAMMATORY ACTIVITY; APOPTOSIS; ARTICLE; CAPILLARY DENSITY; CONTROLLED STUDY; CORONARY ARTERY LIGATION; CYTOKINE PRODUCTION; DRUG EFFECT; DRUG MECHANISM; ECHOCARDIOGRAPHY; HEART INFARCTION; HEART PROTECTION; HISTOLOGY; INFLAMMATION; LEFT ANTERIOR DESCENDING CORONARY ARTERY; LEFT VENTRICULAR SYSTOLIC DYSFUNCTION; MALE; MOUSE; MUSCLE CELL; MYOCARDIAL DISEASE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; VASODILATATION; ANIMAL; BLOOD; C57BL MOUSE; CAPILLARY; CORONARY BLOOD VESSEL; DISEASE MODEL; GENE THERAPY; GENETICS; HEART LEFT VENTRICLE FUNCTION; HEART MUSCLE CELL; INTRAMUSCULAR DRUG ADMINISTRATION; KNOCKOUT MOUSE; METABOLISM; MYOCARDIAL INFARCTION; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY; PROCEDURES; SURGERY; TREATMENT OUTCOME;

MURINAE; MUS;

ADIPONECTIN; ANIMALS; APOPTOSIS; BETA-GALACTOSIDASE; CAPILLARIES; CORONARY VESSELS; CYTOKINES; DISEASE MODELS, ANIMAL; FIBROBLAST GROWTH FACTORS; GENETIC THERAPY; INJECTIONS, INTRAMUSCULAR; MALE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYOCARDIAL INFARCTION; MYOCYTES, CARDIAC; TREATMENT OUTCOME; VENTRICULAR DYSFUNCTION, LEFT;

EID: 84930179198     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2015.02.081     Document Type: Article

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