Related Experiment Video

Updated: May 1, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.1K

AIM2 mediates inflammation-associated renal damage in hepatitis B virus-associated glomerulonephritis by regulating

Junhui Zhen1, Le Zhang2, Jiachao Pan2

  • 1School of Medicine, Shandong University, Jinan 250012, China ; Department of Pathology, School of Medicine, Shandong University, Jinan 250012, China.

Mediators of Inflammation
|April 5, 2014
PubMed
Abstract

Insights

AIM2 inflammasome expression is elevated in hepatitis B virus-associated glomerulonephritis (HBV-GN), correlating with inflammation and renal damage. Reducing AIM2 (absent in melanoma 2) may offer a therapeutic strategy for HBV-GN.

Area of Science:

  • Immunology
  • Virology
  • Nephrology

Background:

  • AIM2 (absent in melanoma 2) is crucial for innate immunity, but its role in hepatitis B virus (HBV) infection is unclear.
  • This study investigates the hypothesis that AIM2 expression correlates with HBV-induced inflammation in HBV-associated glomerulonephritis (HBV-GN), contributing to kidney damage.

Purpose of the Study:

  • To analyze AIM2 expression in HBV-GN tissues and cell lines.
  • To determine the correlation between AIM2, inflammatory factors, and HBV status.
  • To evaluate the impact of AIM2 on the inflammatory response to HBV infection.

Main Methods:

  • Immunohistochemistry was used to detect AIM2, caspase-1, and IL-1β in renal biopsies from 79 patients (54 HBV-GN, 24 CGN).
  • AIM2 was knocked down using siRNA in human glomerular mesangial (HGM) cells infected with HBV.
  • qRT-PCR and Western blot analyzed the expression of caspase-1, IL-1β, and IL-18 post-AIM2 knockdown.

Main Results:

  • AIM2 expression was significantly higher in HBV-GN biopsies (81.4%) compared to CGN (4.0%).
  • AIM2 expression positively correlated with caspase-1 and IL-1β levels in HBV-GN patients.
  • AIM2 knockdown reduced caspase-1, IL-1β, and IL-18 expression in both HBV-infected and uninfected HGM cells.

Conclusions:

  • Elevated AIM2 during HBV infection or replication may exacerbate inflammatory damage in HBV-GN.
  • AIM2 presents a potential therapeutic target for managing HBV-associated glomerulonephritis.

More Related Videos

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection10:15

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Published on: November 10, 2021

1.8K

Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
52
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal...
34
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to...
42
Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver.
86
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.2K
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
12.5K