期刊
INTERACTIVE CARDIOVASCULAR AND THORACIC SURGERY
卷 11, 期 4, 页码 455-460出版社
OXFORD UNIV PRESS
DOI: 10.1510/icvts.2010.234773
关键词
Bone morphogenetic proteins; Cardiac diseases; Signal transduction; Smad proteins; Transforming growth factor-beta; MAP kinase signaling system
The transforming growth factor-beta (TGF-beta) superfamily are of structurally related proteins that mediate developmental processes including cell growth, apoptosis, cellular homeostasis, tissue differentiation, morphogenesis, proliferation, and migration. Smads are intracellular signaling effectors that mediate intracellular signaling of the TGF-beta superfamily. They have been implicated in a wide range of cardiac disorders, including cardiac failure, cardiac fibrosis, myocardial infarction, injury induced by angioplasty, and pulmonary artery hypertension. They also have a function to regulate cardiac structural development in embryos. By binding to types I and II of serine-threonine kinase receptors, bone morphogenetic protein 2 (BMP2) enables phosphorylation of Smad1 to form hetero-oligomeric complexes with Smad4, and modulate the transcription of the target genes after they are translocated into the nucleus. Appropriate interventions, such as Smad-responsive transcriptional promoter and antifibrotic angiotensin-converting enzyme inhibitors, can be helpful in reversing cardiac abnormalities. The aim of this article is to describe the current research results of Smad proteins in terms of cardiac disorders and development through transforming growth factor (TGF)-beta pathways. (C) 2010 Published by European Association for Cardio-Thoracic Surgery. All rights reserved.
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