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ISSN: 2157-7099

Journal of Cytology & Histology
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Review Article

The Role of TGF-β Signaling in β-Cell Dysfunction and Type 2 Diabetes: A Review

Shane Fischbach1,2 and George K. Gittes1*

1Division of Pediatric Surgery, Children’s Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA 15224, USA

2Division of Biology and Medicine, Brown University, Providence, RI, 02912, USA

*Corresponding Author:
George K. Gittes
Division of Pediatric General and Thoracic Surgery
4401 Penn Avenue, Pittsburgh, PA 15224, USA
Tel: (412) 692-7280
Fax: (412) 692-6069
E-mail: [email protected]

Received Date: August 14, 2014; Accepted Date: September 27, 2014; Published Date: September 29, 2014

Citation: Fischbach S, Gittes GK (2014) The Role of TGF-ß Signaling in ß-Cell Dysfunction and Type 2 Diabetes: A Review. J Cytol Histol 5:282. doi:10.4172/2157-7099.1000282

Copyright: © 2014 Fischbach S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Type 2 Diabetes (T2D) is a global epidemic that affects hundreds of millions of individuals. The pancreatic β-cell has long been the focus of studies pertaining to T2D, but the therapies that exist to date are inadequate. Devising new therapies will require a more detailed understanding of the pathogenesis of T2D and of the normal function of the β-cell. In particular, there is a great need to understand the signaling pathways that govern normal β-cell function and that become dysfunctional during the progression to diabetes. The Transforming Growth Factor β (TGF-β) signaling pathway is implicated in nearly all tissue types in the body, and has been shown to play a role in pancreas development and homeostasis, including β-cell regeneration after pancreatic insult. TGF-β exerts its cellular effects through transcriptional activity of downstream SMAD molecules, as well as through cross-talk with other signaling pathways. Accumulating evidence suggests that β-cell failure in T2D is a multifaceted process that may include islet inflammation, increased β-cell apoptosis, reduced β-cell proliferation, and/or β-cell dedifferentiation to a progenitorlike state. This review details the known roles of TGF-β signaling in dedifferentiation-induced and inflammationinduced β-cell failure, and draws on the apparent coordinated regulation of β-cell proliferation and the β-cell differentiation state to offer new hypotheses about β-cell failure in T2D.

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