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MicroRNAs and fibrosis
Journal article   Peer reviewed

MicroRNAs and fibrosis

Vishal Patel and Lama Noureddine
Current opinion in nephrology and hypertension, Vol.21(4), pp.410-416
07/2012
DOI: 10.1097/MNH.0b013e328354e559
PMCID: PMC3399722
PMID: 22622653
url
https://www.ncbi.nlm.nih.gov/pmc/articles/3399722View
Open Access

Abstract

MicroRNAs (miRNAs) are short noncoding RNAs that inhibit gene expression in plants and animals. miRNAs have emerged as key players in virtually all aspects of mammalian biology. Aberrant miRNA expression is observed in numerous human diseases such as diabetes, hypercholesterolemia, cancer, and tissue fibrosis. Therefore, approaches to correct miRNA expression represent the novel therapeutic strategies for these diseases. miRNAs are essential for kidney development and homeostasis. Aberrant miRNA expression is observed in the mouse models of kidney fibrosis. Three TGF-β-regulated miRNA families, miR-21, miR-200, and miR-29 have been shown to modulate renal fibrosis. miR-21, through a feed-forward loop, amplifies TGF-β signaling and promotes fibrosis. Conversely, miR-200 and miR-29 reduce fibrosis by inhibiting epithelial-to-mesenchymal transition and preventing the deposition of extracellular matrix, respectively. Inhibition of miR-21 expression or augmenting miR-29 expression prevents kidney fibrosis in mice. Aberrant miRNA expression perturbs signaling pathways that lead to progression of kidney fibrosis. Thus, miRNAs represent novel biomarkers and therapeutic targets in the treatment of kidney fibrosis.
Genetic Markers MicroRNAs - therapeutic use Genetic Therapy Kidney - pathology Kidney Diseases - pathology Humans Gene Expression Regulation MicroRNAs - metabolism Kidney Diseases - genetics Kidney - metabolism Animals Fibrosis Kidney Diseases - therapy Transforming Growth Factor beta - metabolism Kidney Diseases - metabolism

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