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Review
. 2017 May 15:9:36.
doi: 10.1186/s13098-017-0233-1. eCollection 2017.

Mesenchymal stem cell therapy in type 2 diabetes mellitus

Affiliations
Review

Mesenchymal stem cell therapy in type 2 diabetes mellitus

Li Zang et al. Diabetol Metab Syndr. .

Abstract

Type 2 diabetes mellitus (T2DM), which is characterized by the combination of relative insulin deficiency and insulin resistance, cannot be reversed with existing therapeutic strategies. Transplantation of insulin-producing cells (IPCs) was once thought to be the most promising strategy for treating diabetes, but the pace from the laboratory to clinical application has been obstructed due to its drawbacks. Mesenchymal stem cells (MSCs) harbor differentiation potential, immunosuppressive properties, and anti-inflammatory effects, and they are considered an ideal candidate cell type for treatment of DM. MSC-related research has demonstrated exciting therapeutic effects in glycemic control both in vivo and in vitro, and these results now have been translated into clinical practice. However, some critical potential problems have emerged from current clinical trials. Multi-center, large-scale, double-blind, and placebo-controlled studies with strict supervision are required before MSC transplantation can become a routine therapeutic approach for T2DM. We briefly review the molecular mechanism of MSC treatment for T2DM as well as the merits and drawbacks identified in current clinical trials.

Keywords: Insulin resistance; Mesenchymal stem cells; Type 2 diabetes mellitus.

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Figures

Fig. 1
Fig. 1
Diagram explaining the mechanism by which MSCs act on type 2 diabetes. MSCs exert beneficial effects on type 2 diabetes through differentiation into IPCs, promotion of islet cell regeneration, protection of endogenous islet cells and amelioration of insulin resistance. IPCs insulin-producing cells, IGF-1 insulin-like growth factor-1, VEGF vascular endothelial growth factor, PDGF platelet-derived growth factor, IRS-1 insulin receptor substrate-1, PI3K phosphoinositide 3-kinase

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