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A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model
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A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model

Published on: September 11, 2020

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CircMTO1 Attenuated Acute Kidney Injury Through Regulating miR-337

Chuan-Chuan Shi1, Lu-Yan Pan2, Zhi-Yong Peng1

  • 1Department of Intensive Care Unit, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, China.

Inflammation
|March 12, 2020
PubMed

Insights

This study reveals that circular RNA circMTO1 is decreased in sepsis-induced acute kidney injury (AKI). Upregulating circMTO1 may protect against sepsis-induced AKI by regulating miR-337 and KLF6.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathology

Background:

  • Sepsis-induced acute kidney injury (AKI) significantly increases mortality risk.
  • Understanding the molecular mechanisms of sepsis-induced AKI is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role and mechanism of circMTO1 in sepsis-induced AKI.
  • To explore circMTO1's potential as a therapeutic target for sepsis-induced AKI.

Main Methods:

  • Investigated circMTO1 expression in sepsis-induced AKI rat models and lipopolysaccharide (LPS)-treated rat myocardial cells (RMCs).
  • Utilized bioinformatics analysis to identify molecular interactions.
  • Assessed the effects of circMTO1 overexpression on cell viability, apoptosis, and cytokine production.

Main Results:

  • CircMTO1 expression was significantly reduced in sepsis-induced AKI models and LPS-treated RMCs.
  • Overexpression of circMTO1 enhanced RMC viability, reduced apoptosis, and suppressed cytokine production.
  • Bioinformatics analysis indicated circMTO1 acts as a sponge for miR-337 and inhibits KLF6 expression.

Conclusions:

  • CircMTO1 expression is downregulated in sepsis-induced AKI.
  • CircMTO1 overexpression attenuates sepsis-induced AKI by sponging miR-337 and regulating KLF6.
  • CircMTO1 represents a potential therapeutic target for sepsis-induced AKI.

Keywords:
AKIKLF6circMTO1miR-337sepsis

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