Mitochondrial ACOD1/IRG1 in infection and sterile inflammation

Runliu Wu, Rui Kang, Daolin Tang

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations


Immunometabolism is a dynamic process involving the interplay of metabolism and immune response in health and diseases. Increasing evidence suggests that impaired immunometabolism contributes to infectious and inflammatory diseases. In particular, the mitochondrial enzyme aconitate decarboxylase 1 (ACOD1, best known as immunoresponsive gene 1 [IRG1]) is upregulated under various inflammatory conditions and serves as a pivotal regulator of immunometabolism involved in itaconate production, macrophage polarization, inflammasome activation, and oxidative stress. Consequently, the activation of the ACOD1 pathway is implicated in regulating the pathogenic process of sepsis and septic shock, which are part of a clinical syndrome of life-threatening organ failure caused by a dysregulated host response to pathogen infection. In this review, we discuss the latest research advances in ACOD1 expression and function, with particular attention to how the ACOD1-itaconate pathway affects infection and sterile inflammation diseases. These new insights may give us a deeper understanding of the role of immunometabolism in innate immunity.

Original languageEnglish (US)
Pages (from-to)78-88
Number of pages11
JournalJournal of Intensive Medicine
Issue number2
StatePublished - Apr 2022


  • Aconitate decarboxylase 1 (ACOD1)
  • Disease
  • Inflammation
  • Metabolism
  • Sepsis

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine


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