Format

Send to

Choose Destination
See comment in PubMed Commons below
Interact Cardiovasc Thorac Surg. 2010 Oct;11(4):455-60. doi: 10.1510/icvts.2010.234773. Epub 2010 Jul 22.

Cardiac pathologies in relation to Smad-dependent pathways.

Author information

1
Department of Cardiothoracic Surgery, Jinling Hospital, School of Clinical Medicine, Nanjing University, Nanjing 210002, Jiangsu Province, China.

Abstract

The transforming growth factor-β (TGF-β) 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-β 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)-β pathways.

PMID:
20650957
DOI:
10.1510/icvts.2010.234773
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Silverchair Information Systems
    Loading ...
    Support Center