Suppression of TGF-β1/Smad signaling pathway by sesamin contributes to the attenuation of myocardial fibrosis in spontaneously hypertensive rats

PLoS ONE

Volumn 10, Issue 3, 2015, Pages

  Zhao, Mengqiu ^a   Zheng, Shuguo ^a   Yang, Jieren ^a   Wu, Yuanjie ^b   Ren, Younan ^a   Kong, Xiang ^a   Li, Wei ^a   Xuan, Jiali ^a  

^a WANNAN MEDICAL COLLEGE   (China)

^b ANHUI UNIVERSITY OF CHINESE MEDICINE   (China)

Author keywords

[No Author keywords available]

Indexed keywords

ANGIOTENSIN II; CAPTOPRIL; COLLAGEN; COLLAGEN TYPE 1; COLLAGEN TYPE 3; MALONALDEHYDE; P47PHOX PROTEIN; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE; SESAMIN; SMAD PROTEIN; SMAD3 PROTEIN; SMAD7 PROTEIN; SUPEROXIDE DISMUTASE; TRANSFORMING GROWTH FACTOR BETA1; UNCLASSIFIED DRUG; 1,3 DIOXOLANE DERIVATIVE; ANTIOXIDANT; LIGNAN; NEUTROPHIL CYTOSOLIC FACTOR 1;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DOSE RESPONSE; DRUG MECHANISM; DRUG MEGADOSE; HEART LEFT VENTRICLE HYPERTROPHY; HEART LEFT VENTRICLE MASS; HEART MUSCLE FIBROSIS; HYPERTENSION; LOW DRUG DOSE; MALE; NONHUMAN; PROTEIN LOCALIZATION; PROTEIN PHOSPHORYLATION; PROTEIN SECRETION; RAT; SIGNAL TRANSDUCTION; SYSTOLIC BLOOD PRESSURE; ANIMAL; BLOOD; BLOOD PRESSURE; CARDIAC MUSCLE; DRUG EFFECTS; FIBROBLAST; FIBROSIS; HEART VENTRICLE; METABOLISM; ORGAN SIZE; PATHOLOGY; PATHOPHYSIOLOGY; PHOSPHORYLATION; SPONTANEOUSLY HYPERTENSIVE RAT; SYSTOLE;

RATTUS;

ANGIOTENSIN II; ANIMALS; ANTIOXIDANTS; BLOOD PRESSURE; COLLAGEN TYPE I; COLLAGEN TYPE III; DIOXOLES; FIBROBLASTS; FIBROSIS; HEART VENTRICLES; LIGNANS; MALE; MALONDIALDEHYDE; MYOCARDIUM; NADPH OXIDASE; ORGAN SIZE; PHOSPHORYLATION; RATS, INBRED SHR; SIGNAL TRANSDUCTION; SMAD3 PROTEIN; SMAD7 PROTEIN; SUPEROXIDE DISMUTASE; SYSTOLE; TRANSFORMING GROWTH FACTOR BETA1;

EID: 84925842665     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0121312     Document Type: Article

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