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angiotensinogen gene transcription in pulmonary fibrosis在肺纤维化血管紧张肽原基因转录
Hindawi Publishing Corporation
International Journal of Peptides
Volume 2012, Article ID 875910, 8 pages
doi:10.1155/2012/875910
Review Article
Angiotensinogen Gene Transcription in Pulmonary Fibrosis
Bruce D. Uhal,1 My-Trang T. Dang,1 Xiaopeng Li,2 and Amal Abdul-Hafez3
1 Department of Physiology, Michigan State University, 2201 Biomedical and Physical Sciences Building,
East Lansing, MI 48824, USA
2 Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA
3 College of Pharmacy, Misr International University, Cairo 11331, Egypt
Correspondence should be addressed to Bruce D. Uhal, uhal@
Received 20 October 2011; Accepted 8 December 2011
Academic Editor: Jean-Marie Zajac
Copyright © 2012 Bruce D. Uhal et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
An established body of literature supports the hypothesis that activation of a local tissue angiotensin (ANG) system in the
extravascular tissue compartment of the lungs is required for lung fibrogenesis. Transcriptional activation of the angiotensinogen
(AGT) gene is believed to be a critical and necessary step in this activation. This paper summarizes the data in support of this
theory and discusses transcriptional regulation of AGT, with an emphasis on lung AGT synthesis as a determinant of fibrosis
severity. Genetic data linking AGT polymorphisms to the severity of disease in Idiopathic Pulmonary Fibrosis are also discussed.
1. Introduction to the circulating level could not be explained by diffusion
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