Abstract
Diabetes is a global epidemic and affects millions of individuals in the United States. Devising novel treatments for diabetes continues to be a great medical challenge. Postnatal beta cell growth or compensation is largely attributed to beta cell proliferation, which declines continuously with age. To boost beta cell proliferation to regenerate an adequate functional mass, there is a need to understand the signaling pathways that regulate beta cell proliferation for creating practical strategies to promote the process. Transforming growth factor β (TGFβ) belongs to a signaling superfamily that governs pancreatic development and the regeneration of beta cells after pancreatic diseases. TGFβ exerts its functions by activation of downstream Smad proteins and through its crosstalk with other pathways. Accumulating data demonstrate that the TGFβ receptor signaling pathway also participates in the control of beta cell proliferation. This review details the role of the TGFβ receptor signaling pathway in beta cell proliferation physiologically and in the pathogenesis of diabetes.
Highlights
Insulin is a key regulator of glucose homeostasis, and is produced exclusively by pancreatic beta cells
Inadequate secretion or action of insulin causes diabetes, a metabolic disease characterized by high blood glucose, persistence of which will lead to the classical symptoms of polyuria, polydipsia and polyphagia [1]
Whereas the intestine relies on specialized stem cells to replenish and repair tissue cells, a stem cell appears to be absent in the pancreas [65]
Summary
Insulin is a key regulator of glucose homeostasis, and is produced exclusively by pancreatic beta cells. The TGFβ receptor signaling effects on beta cell manner [5].manner signaling pathway haspathway effects onhas beta cell proliferation proliferation andinphenotype in mouse models. Shown that Smad, potent suppressor of suppressor of TGFβ receptor signaling, plays an essential role in maintenance of beta cell mass and TGFβ receptor signaling, plays an essential role in maintenance of beta cell mass and in postnatal in postnatal beta cell proliferation under certain circumstances. In this on the beta cell proliferation under certain circumstances [6,7,8].
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