Abstract
Diabetic polyneuropathy (DPN) is the most common complication that emerges early in diabetic patients. Intervention with strict blood glucose control or treatment with aldose reductase inhibitor is reported to be effective in early stages of DPN. Curative treatment for overt or symptomatic DPN, however, has not been established, thus requiring much effort to explore a new therapy. Recent preclinical studies on the use of gene or cell therapy have provided promising results in the treatment of DPN. Of particular interest, induced pluripotent stem cells are introduced. In these studies, restoration of DPN was proposed to be attributed to either neurotrophic factors released from transplanted stem cells or differentiation of stem cells to substitute the damaged peripheral nerve. There are still several problems, however, that remain to be overcome, such as perturbed function, fragility, or limited survival of transplanted cells in diabetes milieu and risk for malignant transformation of transplanted cells. Questions, which cell is the most appropriate as the source for cell therapy, or which site is the best for transplantation to obtain the most effective results, remain to be answered. In this communication, we overview the current status of preclinical studies on the cell therapy for DPN and discuss the future prospect.
Highlights
Diabetic polyneuropathy (DPN) is an early and frequent complication of diabetes
Population of small fibers in the skin observed by confocal laser scan microscopy is found to be dramatically reduced in patients with impaired glucose tolerance, pre-diabetic stage of type 2 diabetic patients [2]
It is likely that there is almost no patient who does not suffer from incipient progression of nerve damage in the presence of diabetes
Summary
Diabetic polyneuropathy (DPN) is an early and frequent complication of diabetes. Before symptoms become evident, most diabetic patients exhibit more or less abnormal peripheral nerve function such as prolonged F wave latency or reduced nerve conduction velocity of sural and tibial nerves, indicative of early metabolic interference to nerve integrity [1]. Underlying pathology of diabetic neuropathy is characterized by a progressive distal axonal degeneration, axonal loss, and demyelination [3, 4] accompanied by microvascular changes, which exhibit typical features of microangiopathy with thickening of basement membrane and luminal occlusion [5,6,7]. Under such circumstances, peripheral nerve tissues undergo ischemia and poor supply of nerve nutrients as well as nerve trophic factors, contributing to development of neuropathy. 1 × 106 number of CB-EPC were transplanted into quadriceps muscle, www.frontiersin.org
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