Diabetic polyneuropathy is a common and disturbing complication of diabetes mellitus, presenting patients and caregivers with a substantial disease burden. Emerging mechanisms which are underlying diabetes may provide novel pathways to understand diabetic polyneuropathy (DPN). Specifically, non-coding RNA molecules consisting of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are implicated in the biological processes underlying DPN, and may link it to clinical spheres such as other metabolic and neural pathologies. Here, we elaborate on several candidate non-coding RNAs which may be associated with DPN via regulatory roles governing phenomena related to inflammatory, pain-provoking, and metabolic syndrome pathways. Specific examples include miRNAs such as miR-106a, -146a, -9, -29b, -466a, and -98; likewise, lncRNAs MIAT, PVT1, H19, MEG3, and MALAT1 are implicated, often co-affecting the involved pathways. Incorporating newly discovered regulators into what we know about specific clinical applications may highlight novel avenues for diagnosis, prevention, and intervention with DPN.
Keywords: Diabetes; Fibromyalgia; Long non-coding RNAs; MicroRNAs; Polyneuropathy; Sponging activities.
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