MicroRNAs and fibrosis

Vishal Patel, Lama Noureddine

Research output: Contribution to journalArticle

111 Citations (Scopus)

Abstract

Purpose of review: 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. Recent findings: 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. Summary: 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.

Original languageEnglish (US)
Pages (from-to)410-416
Number of pages7
JournalCurrent Opinion in Nephrology and Hypertension
Volume21
Issue number4
DOIs
StatePublished - Jul 2012

Fingerprint

MicroRNAs
Fibrosis
Kidney
Small Untranslated RNA
Epithelial-Mesenchymal Transition
Hypercholesterolemia
Extracellular Matrix
Homeostasis
Biomarkers
Gene Expression
Therapeutics

Keywords

  • kidney fibrosis
  • microRNA
  • miR-200
  • miR-21
  • miR-29

ASJC Scopus subject areas

  • Nephrology
  • Internal Medicine

Cite this

MicroRNAs and fibrosis. / Patel, Vishal; Noureddine, Lama.

In: Current Opinion in Nephrology and Hypertension, Vol. 21, No. 4, 07.2012, p. 410-416.

Research output: Contribution to journalArticle

Patel, Vishal ; Noureddine, Lama. / MicroRNAs and fibrosis. In: Current Opinion in Nephrology and Hypertension. 2012 ; Vol. 21, No. 4. pp. 410-416.
@article{d1950cc4ea374bf4846cf2d4cd791645,
title = "MicroRNAs and fibrosis",
abstract = "Purpose of review: 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. Recent findings: 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. Summary: 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.",
keywords = "kidney fibrosis, microRNA, miR-200, miR-21, miR-29",
author = "Vishal Patel and Lama Noureddine",
year = "2012",
month = "7",
doi = "10.1097/MNH.0b013e328354e559",
language = "English (US)",
volume = "21",
pages = "410--416",
journal = "Current Opinion in Nephrology and Hypertension",
issn = "1062-4821",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - MicroRNAs and fibrosis

AU - Patel, Vishal

AU - Noureddine, Lama

PY - 2012/7

Y1 - 2012/7

N2 - Purpose of review: 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. Recent findings: 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. Summary: 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.

AB - Purpose of review: 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. Recent findings: 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. Summary: 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.

KW - kidney fibrosis

KW - microRNA

KW - miR-200

KW - miR-21

KW - miR-29

UR - http://www.scopus.com/inward/record.url?scp=84862118082&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84862118082&partnerID=8YFLogxK

U2 - 10.1097/MNH.0b013e328354e559

DO - 10.1097/MNH.0b013e328354e559

M3 - Article

VL - 21

SP - 410

EP - 416

JO - Current Opinion in Nephrology and Hypertension

JF - Current Opinion in Nephrology and Hypertension

SN - 1062-4821

IS - 4

ER -