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Non-Coding Rna-Mediated Epigenetic Alterations in Grave's Ophthalmopathy: A Scoping Systematic Review Publisher



Shahraki K1, 2 ; Pak VI1 ; Najafi A3 ; Shahraki K1, 2 ; Boroumand PG5 ; Sheervalilou R6
Authors
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Authors Affiliations
  1. 1. Ocular Tissue Engineering Research Center, Ophthalmic Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  2. 2. Department of Ophthalmology, Zahedan University of Medical Sciences, Zahedan, Iran
  3. 3. Department of Ophthalmology, Ardabil University of Medical Sciences, Ardabil, Iran
  4. 4. Cornea Department, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. ENT, Head and Neck Research Center and Department, Iran University of Medical Science, Tehran, Iran
  6. 6. Pharmacology Research Center, Zahedan University of Medical Sciences, Zahedan, Iran

Source: Non-coding RNA Research Published:2023


Abstract

Background: It is becoming more and more apparent that Grave's Ophthalmopathy (GO) pathogenesis may be aided by epigenetic processes such as DNA methylation modifications, histone tail covalent modifications, and non-coding RNA (ncRNA)-based epigenetic processes. In the present study, we aimed to focus more on the miRNAs rather than lncRNAs due to lack of investigations on these non-coding RNAs and their role in GO's pathogenesis. Methods: A six-stage methodology framework and the PRISMA recommendation were used to conduct this scoping review. A comprehensive search was conducted across seven databases to discover relevant papers published until February 2022. The data extraction separately, and quantitative and qualitative analyses were conducted. Results: A total of 20 articles were found to meet inclusion criteria. According to the results, ncRNA were involved in the regulation of inflammation (miR-146a, LPAL2/miR-1287–5p axis, LINC01820:13/hsa miR-27b-3p axis, and ENST00000499452/hsa-miR-27a-3p axis), regulation of T cell functions (miR-146a/miR-183/miR-96), regulation of glycosaminoglycan aggregation and fibrosis (miR-146a/miR-21), glucocorticoid sensitivity (miR-224–5p), lipid accumulation and adipogenesis (miR-27a/miR-27b/miR-130a), oxidative stress and angiogenesis (miR-199a), and orbital fibroblast proliferation (miR-21/miR-146a/miR-155). Eleven miRNAs (miR-146a/miR-224–5p/miR-Let7d-5p/miR-96–5p/miR-301a-3p/miR-21–5p) were also indicated to have the capacity to be used as biomarkers. Conclusions: Regardless of the fact that there is significant documentation of ncRNA-mediated epigenetic dysfunction in GO, additional study is needed to thoroughly comprehend the epigenetic connections concerned in disease pathogenesis, paving the way for novel diagnostic and prognostic tools for epigenetic therapies among the patients. © 2023 The Authors
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