Role of miRNA and lncRNAs in organ fibrosis and aging

Biomed Pharmacother. 2021 Nov:143:112132. doi: 10.1016/j.biopha.2021.112132. Epub 2021 Sep 1.

Abstract

Fibrosis is the endpoint of pathological remodeling. This process contributes to the pathogenesis of several chronic disorders and aging-associated organ damage. Different molecular cascades contribute to this process. TGF-β, WNT, and YAP/TAZ signaling pathways have prominent roles in this process. A number of long non-coding RNAs and microRNAs have been found to regulate organ fibrosis through modulation of the activity of related signaling pathways. miR-144-3p, miR-451, miR-200b, and miR-328 are among microRNAs that participate in the pathology of cardiac fibrosis. Meanwhile, miR-34a, miR-17-5p, miR-122, miR-146a, and miR-350 contribute to liver fibrosis in different situations. PVT1, MALAT1, GAS5, NRON, PFL, MIAT, HULC, ANRIL, and H19 are among long non-coding RNAs that participate in organ fibrosis. We review the impact of long non-coding RNAs and microRNAs in organ fibrosis and aging-related pathologies.

Keywords: Aging; LncRNA; MiRNA; Organ fibrosis.

Publication types

  • Review

MeSH terms

  • Aging / genetics
  • Aging / metabolism*
  • Aging / pathology
  • Animals
  • Cardiomyopathies / genetics
  • Cardiomyopathies / metabolism*
  • Cardiomyopathies / pathology
  • Fibrosis
  • Gene Expression Regulation
  • Humans
  • Kidney Diseases / genetics
  • Kidney Diseases / metabolism*
  • Kidney Diseases / pathology
  • Liver Cirrhosis / genetics
  • Liver Cirrhosis / metabolism*
  • Liver Cirrhosis / pathology
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Pulmonary Fibrosis / genetics
  • Pulmonary Fibrosis / metabolism*
  • Pulmonary Fibrosis / pathology
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • Signal Transduction

Substances

  • MicroRNAs
  • RNA, Long Noncoding