Please use this identifier to cite or link to this item:
https://hdl.handle.net/20.500.14365/2587
Title: | Role of the Microrna-29 Family in Fibrotic Skin Diseases | Authors: | Harmancı, Duygu Erkan, Erdogan Pekcan Kocak, Ayse Akdoğan, Gül |
Keywords: | microRNA-29 family skin fibrotic skin diseases function pathogenesis Systemic-Sclerosis Pulmonary-Fibrosis Liver Fibrosis Extracellular-Matrix Hypertrophic Scars Mir-29 Expression Apoptosis Pathway Suppression |
Publisher: | Spandidos Publ Ltd | Abstract: | Fibrotic skin diseases are characterized by the accumulation of collagen. The hallmarks of fibrotic skin diseases are unbalanced fibroblast proliferation and differentiation, extracellular matrix production and transforming growth factor- signalling. Numerous studies have investigated the possibility that microRNAs (miRNAs or miRs) are involved in the pathogenesis of certain fibrotic diseases, including skin, heart, lung and liver diseases. miRNAs are a class of small non-coding RNAs, which modify gene expression by binding to target messenger RNA (mRNA) and blocking the translation or inducing the degradation of target mRNA. The biological relevance of miRNAs has been investigated in physiological and pathological conditions, and there is increasing evidence that the miR-29 family is associated with fibrotic diseases. The aim of the present review is to provide an up-to-date summary of current knowledge on the latest developments associated with the miR-29 family and fibrotic skin diseases. | URI: | https://doi.org/10.3892/br.2017.900 https://hdl.handle.net/20.500.14365/2587 |
ISSN: | 2049-9434 2049-9442 |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
Show full item record
CORE Recommender
WEB OF SCIENCETM
Citations
32
checked on Dec 18, 2024
Page view(s)
130
checked on Dec 16, 2024
Download(s)
24
checked on Dec 16, 2024
Google ScholarTM
Check
Altmetric
Items in GCRIS Repository are protected by copyright, with all rights reserved, unless otherwise indicated.