Bone Marrow-Derived Mesenchymal Stem Cells Improve Diabetic Neuropathy by Direct Modulation of Both Angiogenesis and Myelination in Peripheral Nerves

Han, Ji Yun; Choi, Dawoon; Lee, Min Young; Huh, Yang Hoon; Yoon, Young Sup

doi:10.3727/096368915x688209

Cited by 80 publications

(70 citation statements)

References 57 publications

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“…Interestingly, inside the nerve parenchyma, ADSCs were detected in close proximity to intraneuronal vessels. Similar findings were demonstrated by Han et al after intramuscular injection of bone‐marrow derived MSCs (BM‐MSCs) in a diabetic neuropathy rat model . Stem cells were preferentially engrafted in the nerve parenchyma and partly localized in close proximity to vasa nervora of sciatic nerves.…”

Section: Discussionsupporting

confidence: 82%

ADSCs in a fibrin matrix enhance nerve regeneration after epineural suturing in a rat model

et al. 2015

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Section: Discussionsupporting

confidence: 82%

ADSCs in a fibrin matrix enhance nerve regeneration after epineural suturing in a rat model

et al. 2015

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“…Several therapeutic strategies are being pursued to manipulate nerve plasticity and neurite outgrowth in diabetes, with the aim of encouraging axonal repair [161][162][163] . A study published in 2016 identified p75NTR as a novel therapeutic target in type 2 diabetes, on the basis of results using an adipocyte-specific conditional null mouse model shown to be resilient to high-fat-diet-induced obesity and insulin resistance 164 .…”

Section: Impact Of Schwannopathy On Neuronsmentioning

confidence: 99%

Schwann cell interactions with axons and microvessels in diabetic neuropathy

et al. 2017

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The incidence of diabetes mellitus has increased dramatically over the past two to three decades. According to the International Diabetes Federation Diabetes Atlas, 415 million people worldwide had diabetes in 2015, and this number is expected to grow by 5% annually, predominantly as a result of increasing prevalence of type 2 diabetes. Furthermore, an estimated 100 million Europeans and 80 million Americans have impaired glucose tolerance or prediabetes. Few people die from acute diabetes in countries with comprehensive health care systems, but the disease is inflicting a huge medical, social and economic burden on society owing to the need for lifelong treatment of its systemic consequences and the insidious development of multi-organ damage.Peripheral neuropathy (BOXES 1,2) is a common but often neglected complication of long-term diabetes, and the lack of treatment options reflects an incomplete understanding of the pathogenic mechanisms. Hyperglycaemia is generally accepted as the primary pathogenic insult in type 1 and type 2 diabetic neuropathy, although roles are emerging for other factors, such as impaired insulin signalling, hypertension and dyslipidaemia (particularly for type 2 diabetes), which might precede overt hyperglycaemia 1 . Many preclinical studies, and occasional clinical studies, have indicated that diabetic neuropathy -like diabetic nephropathy and retinopathy -results from microvascular disease, with a focus on axonal degeneration as a consequence of ischaemia and/or hypoxia. This mechanism, however, is likely to be only one aspect of a more complex pathogenesis.The earliest descriptions of pathology in diabetic neuropathy indicated that Schwannopathy accompanied axonal degeneration. The majority of clinical and basic research in diabetic neuropathy since then has focused on the effects on neurons. However, accumulating data from research into the development and regeneration of the PNS has identified Schwann cells as equally indispensable components that maintain neuronal structure and function, nourish axons, and promote survival and growth upon injury. The early reports from 1979 that demonstrated morphological changes in Schwann cells in human diabetic neuropathy 2 are now supported by an increased awareness of molecular alterations in Schwann cells during diabetes 3 . Schwann cells express a wide range of receptors and, when they sense insults or danger signals, they upregulate synthesis and secretion of factors that stimulate neuroprotection, regrowth and remyelination, or factors that aggravate disease phenotypes 4 . The most recent studies have demonstrated that Schwann cells regulate many aspects of axonal function, so that disruption of their metabolism by diabetes results in the accumulation of neurotoxic intermediates and compromises production of neuronal support factors, contributing to axonal degeneration, endothelial dysfunction and diabetic neuropathy. Abstract | The prevalence of diabetes worldwide is at pandemic levels, with the number of patients increasing by 5% annu...

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“…Bueno and colleagues also demonstrated improved insulin sensitivity in diabetic rats induced by a hyperlipidic diet and treated with MSCs intraperitoneally. The action of MSCs on insulin sensitivity in these studies is probably associated with their immunomodulatory role . No findings were analyzed in models with type 1 DM.…”

Section: Discussionmentioning

confidence: 90%