Abstract
Diabetic neuropathy is a serious complication of chronic hyperglycemia in diabetes patients. This complication can involve both peripheral sensorimotor and autonomic nervous system. The precise nature of injury to the peripheral nerves mediated by chronic hyperglycemia is unknown; however, several mechanisms have been proposed including polyol pathway activation, enhanced glycation of proteins and lipids, increased oxidative stress, and cytokine release in the site of injury. MicroRNAs (miRNAs) are small non-coding RNAs that mediate RNA interference by post-transcriptionally modulating gene expression and protein synthesis. Therefore, they have been implicated in several developmental, physiological, and pathophysiological processes where they modulate the expression of different proteins. Recently, miRNAs gained an increasing attention also for their role as diagnostic test in many diseases due to their stability in serum and their easy detection. Furthermore, recent studies suggest that miRNAs may be involved in diabetic neuropathy although their role in the onset and the development of this complication is not fully understood. In this review, we discuss the most recent literature providing evidence for miRNAs role in diabetic neuropathy opening new pathways to improve both early diagnosis and treatment of this complication.
Highlights
Diabetic neuropathy is a serious complication of chronic hyperglycemia in diabetes patients
This upregulation was positively correlated to the expression of calcium homeostasis modulator 1 (CALHM1) even if TargetScan analysis did not confirm this gene as potential target of miR-9
The Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that peroxisome proliferator-activated receptor (PPAR) and adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling pathways were significantly regulated and enriched with PPAR gamma (PPARG), stearoyl-CoA desaturase (SCD), cluster of differentiation 36 (CD36), and phosphoenolpyruvate carboxykinase 1 (PCK1)
Summary
Diabetes mellitus (DM) is a chronic metabolic disease whose incidence worldwide is increasing; overall, about 100 million people are affected. Type 1 diabetes (T1D), defined as insulin-dependent diabetes mellitus, is a multifactorial disorder characterized by the organ-specific autoimmune destruction of pancreatic insulin producing beta cells in human leukocyte antigen (HLA) genetically predisposed subjects [1]. This form occurs in 5%–10% of DM patients [1]. The presence of a chronic inflammatory infiltrate within pancreatic islets leading to insulitis is the main histopathological finding in T1D [2] Another important aspect is that, in patients with longstanding disease, the remaining pancreatic β-cells resistant to autoimmune destruction are incapable of regeneration [3]. We aim to underline the implications of miRNAs in the development of this complication and their potential role as biomarkers and therapeutic targets for future treatments
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