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Acute Kidney Injury V: Interprofessional Care01:20

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Acute Kidney Injury III: Clinical Manifestations01:29

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Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
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Updated: Mar 13, 2026

A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model
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MicroRNA-382 Is Involved in Acute Kidney Injury via Regulating STAT1 Signaling.

Xiaoyan Wang1,2, Guo Cheng2, Ting Ren1

  • 1Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.

Journal of Immunology Research
|March 11, 2026
PubMed
Summary
This summary is machine-generated.

MicroRNA-382 (miR-382) plays a protective role in acute kidney injury (AKI) by reducing inflammation and oxidative stress. Loss of miR-382 worsens kidney damage, while its restoration offers a potential therapeutic strategy for AKI.

Keywords:
acute kidney injurymacrophagesmicroRNAtubular epithelial cells

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Immunology

Background:

  • Acute kidney injury (AKI) is a critical condition involving inflammation and oxidative stress.
  • The role of microRNA-382 (miR-382) in AKI pathogenesis was previously unknown.
  • Chronic kidney disease (CKD) progression has been linked to miR-382.

Purpose of the Study:

  • To investigate the role of miR-382 in the context of acute kidney injury (AKI).
  • To explore the therapeutic potential of miR-382 in AKI models.

Main Methods:

  • Genetic depletion and overexpression of miR-382 in mouse models of ischemia-reperfusion (I/R) and sepsis-induced AKI.
  • In vitro studies using mouse renal tubular epithelial cells (mTECs) and Raw264.7 macrophages subjected to hypoxia/reoxygenation (H/R) and lipopolysaccharide (LPS) treatments.
  • Analysis of STAT1 signaling pathway activation, inflammatory cytokine production (IL-6, TNF-α, IL-1β), reactive oxygen species (ROS), apoptosis, and macrophage polarization.

Main Results:

  • Genetic depletion of miR-382 exacerbated renal dysfunction, inflammation, apoptosis, and oxidative stress in I/R- and sepsis-induced AKI.
  • Downregulation of miR-382 in mTECs correlated with STAT1 activation, increased inflammatory cytokine and ROS production, and apoptosis following H/R and LPS.
  • Overexpression of miR-382 in mTECs attenuated these detrimental effects.
  • Loss of miR-382 was observed in kidney macrophages during I/R-induced AKI.
  • Upregulation of miR-382 in macrophages inhibited STAT1 signaling and M1 polarization, reducing pro-inflammatory mediators.
  • Pharmacological inhibition of STAT1 reduced inflammatory responses in macrophages.

Conclusions:

  • miR-382 exerts a protective effect against ischemia-reperfusion and sepsis-induced AKI.
  • miR-382 functions by suppressing STAT1 signaling, reducing inflammation, oxidative stress, and apoptosis in renal cells and macrophages.
  • miR-382 represents a promising novel therapeutic target for managing AKI.