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Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice
04:47

Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice

Published on: October 27, 2023

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Linking AIM2 Inflammasome Activation, Mitochondrial Dysfunction and Chronic Inflammation in Ankylosing Spondylitis

Catalina Alina Boengiu1, Andreea-Lili Barbulescu2, Cristiana Cerasella Dragomirescu3

  • 1Doctoral School, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.

Cells
|December 10, 2025
PubMed

Insights

The absent in melanoma 2 (AIM2) inflammasome senses DNA and is implicated in ankylosis spondylitis. Targeting AIM2 may offer new therapeutic strategies by addressing mitochondrial dysfunction and autoimmunity.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • The absent in melanoma 2 (AIM2) inflammasome is a cytosolic DNA sensor activated by double-stranded DNA (dsDNA).
  • AIM2 links genomic instability, mitochondrial dysfunction, and chronic inflammation, particularly in autoimmune diseases like ankylosis spondylitis (AS).
  • Current AS therapies do not target upstream mitochondrial dysfunction or DNA-driven inflammasome activation.

Purpose of the Study:

  • To review evidence on AIM2 inflammasome involvement in AS pathogenesis.
  • To explore AIM2 as a potential therapeutic target for AS.
  • To understand AIM2's interaction with inflammation, mitophagy, and oxidative stress in AS.

Main Methods:

  • Literature review of current evidence on AIM2 inflammasome in AS.
  • Analysis of AIM2 activation mechanisms, including dsDNA and mitochondrial DNA (mtDNA) release.
  • Examination of the interplay between AIM2, oxidative stress, mitophagy, and innate immunity.

Main Results:

  • AIM2 is activated by dsDNA, including mtDNA released during stress, positioning it at the nexus of oxidative stress and immune dysregulation.
  • AIM2 inflammasome activation is implicated in the pathogenesis of autoimmune diseases, including AS.
  • AIM2 remains less studied compared to other inflammasomes like NLRP3.

Conclusions:

  • AIM2 activation is a key factor in AS pathogenesis, driven by mitochondrial dysfunction and self-DNA.
  • Targeting the AIM2 inflammasome presents a novel therapeutic avenue for AS.
  • Restoring balance between mitochondrial function and autoimmunity through AIM2 modulation may improve disease control.
Keywords:
AIM2 inflammasomeankylosing spondylitisautoimmunitymitochondrial dysfunctionmtDNAtargeted therapy

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