Non-coding RNA regulators of diabetic polyneuropathy

•Non-coding RNAs (ncRNAs) regulate cellular functions alongside coding elements.•Inflammatory elements are affected by ncRNAs in their regulatory roles.•Numerous ncRNAs mirror clinical associations between diabetes and polyneuropathy.•Both microRNAs and long non-coding RNAs are involved in diabetic...

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Bibliographic Details
Published in:Neuroscience letters 2020-07, Vol.731, p.135058-135058, Article 135058
Main Authors: Meydan, Chanan, Üçeyler, Nurcan, Soreq, Hermona
Format: Article
Language:English
Subjects:
Animals
Cell Proliferation - genetics
Diabetes
Diabetes Mellitus - genetics
Diabetic Neuropathies - genetics
Diabetic Neuropathies - metabolism
Fibromyalgia
Humans
Long non-coding RNAs
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
Polyneuropathy
RNA, Long Noncoding - genetics
Sponging activities
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Summary:•Non-coding RNAs (ncRNAs) regulate cellular functions alongside coding elements.•Inflammatory elements are affected by ncRNAs in their regulatory roles.•Numerous ncRNAs mirror clinical associations between diabetes and polyneuropathy.•Both microRNAs and long non-coding RNAs are involved in diabetic polyneuropathy. 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.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2020.135058