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Protection from renal fibrosis, putative role of TRIB3 gene silencing

Wen-yuan Ding1, Wen-bo Li1, Yun Ti1

  • 1Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Department of Cardiology, Qilu Hospital of Shandong University, Ji'nan 250012, PR China; Department of Cardiology, Qilu Hospital of Shandong University, Ji'nan 250012, PR China.

Experimental and Molecular Pathology
|December 26, 2013
PubMed
Abstract

Insights

Tribbles homolog 3 (TRIB3) overexpression drives renal fibrosis in insulin-resistant rats. Silencing TRIB3 ameliorates kidney fibrosis by reducing extracellular signal-regulated kinase (ERK) phosphorylation, offering a potential therapeutic target for chronic kidney disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathology

Background:

  • Renal fibrosis is a common pathway in chronic kidney disease (CKD).
  • Tribbles homolog 3 (TRIB3) is implicated in cardiac fibrosis during insulin resistance.
  • The role of TRIB3 in renal fibrosis remains unclear.

Purpose of the Study:

  • To investigate the role of TRIB3 in the pathogenesis of renal fibrosis in insulin-resistant rats.
  • To determine if TRIB3 influences key signaling pathways involved in fibrosis.

Main Methods:

  • 40 male Sprague-Dawley rats were divided into control, high-fat diet (HFD), HFD with TRIB3 siRNA, and HFD with vehicle groups.
  • Insulin resistance markers were assessed.
  • Renal tissues were analyzed using histological staining (H&E, Masson's trichrome, PAS).

Main Results:

  • HFD induced insulin resistance and TRIB3 overexpression in rats.
  • TRIB3 upregulation correlated with renal fibrosis and increased extracellular signal-regulated kinase (ERK) phosphorylation.
  • TRIB3 siRNA knockdown attenuated renal fibrosis and decreased ERK phosphorylation.

Conclusions:

  • TRIB3 gene silencing effectively reduces renal fibrosis in a rat model of insulin resistance.
  • TRIB3 plays a significant role in the development of renal fibrosis.
  • Targeting TRIB3 may offer a therapeutic strategy for managing chronic kidney disease.
Keywords:
MAPKRenal fibrosisTRIB3siRNA

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