The Role of TGF-β Receptors in Fibrosis



Sashidhar Nakerakanti , Maria Trojanowska*
Arthritis Center, Boston University School of Medicine, 72 East Concord St, Boston, MA 02118, USA


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© Nakerakanti and Trojanowska; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Arthritis Center, Boston University Medical Center, 72 East Concord St, E-5 Boston, MA 02118, USA; Tel: 617-638-4318; Fax: 617-638-5226; E-mail: trojanme@bu.edu


Abstract

Recent advances in defining TGF-β signaling pathways have provided a new level of understanding of the role of this pleiotropic growth factor in the development of fibrosis. Here, we review selected topics related to the profibrotic role of TGF-β . We will discuss new insights into the mechanisms of ligand activation and the contribution of Erk1/2 MAPK, PI3K/FAK, and Endoglin/Smad1 signaling pathways to the process of fibrosis. There is growing evidence of the disease-specific alterations of the downstream components of the TGF-β signaling pathway that may be explored for the future therapeutic interventions.

Keywords: TGF-β, fibrosis, Erk1/2/MAPK, PI3K, Alk1, Endoglin, Smad1..