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Long non coding RNAs involved in MAPK pathway mechanism mediates diabetic neuropathic pain
Author(s) -
Ren Xinlu,
Yang Runan,
Li Lin,
Xu Xiumei,
Liang Shangdong
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11457
Subject(s) - neuropathic pain , pathogenesis , purinergic receptor , diabetes mellitus , medicine , bioinformatics , long non coding rna , receptor , diabetic neuropathy , neuroscience , downregulation and upregulation , biology , immunology , gene , pharmacology , endocrinology , genetics
Diabetes is the largest global epidemic of the 21st century, and the cost of diabetes and its complications comprise about 12% of global health expenditure. Diabetic neuropathy is the most common complication of diabetes, affecting up to 50% of patients over the course of their disease. Among them, 30%–50% develop neuropathic pain, which has typical symptoms that originate from the toes and progress to foot ulcers and seriously influence quality of life. The pathogenesis of diabetic neuropathic pain (DNP) is complicated and incompletely understood and there is no effective treatment except supportive treatment. Long noncoding RNAs (lncRNAs), a class of noncoding RNAs exceeding 200 nucleotides in length, have been shown to play key roles in fundamental cellular processes, and are considered to be potential targets for treatment. Recent research indicates that lncRNA is involved in the pathogenesis of DNP. Certain overexpressed lncRNAs can enhance the purinergic receptor‐mediated neuropathic pain in peripheral ganglia and inflammatory cytokines are released due to receptors activated by adenosine triphosphate. In recent years, our laboratory also has been exploring the relationship and pathogenesis between lncRNAs and DNP. In this review, we focus on the recent progress in functional lncRNAs associated with DNP and investigate their roles related to respective receptors.