ArticleHepatology communications2026
Itaconate as the endogenous brake of proinflammatory macrophage activation alleviates inflammation in liver fibrogenesis.
Article in Hepatology communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLiver inflammation and fibrosis are reparative responses to chronic liver injury. Bone marrow-derived monocyte/macrophages (BMDMs) are key participants. Our previous study demonstrated that BMDM can be activated as a proinflammatory phenotype by sphingosine-1-phosphate (S1P). Aconitate decarboxylase 1 (ACOD1)/itaconate is an anti-inflammatory molecule. However, it remains unclear whether ACOD1/itaconate is involved in S1P-induced BMDM activation.
methodsA methionine-choline-deficient and high-fat diet was used to induce liver injury and fibrosis in mice. To clarify the role of endogenous ACOD1/itaconate in BMDMs in liver fibrosis, we established 2 types of chimeric mice: (1) bone marrow (BM) Acod1 deficiency (WT or Acod1 knockout BM was transplanted into wild-type mice) and (2) exclusive BM Acod1 expression (WT or Acod1 knockout BM was transplanted into Acod1 knockout mice).
resultsSingle-cell RNA sequencing data revealed that Acod1 was highly expressed in injured BMDMs. Acod1+ BMDMs exhibited a proinflammatory phenotype with elevated expression of proinflammatory genes. In vitro, ACOD1 expression and itaconate production were upregulated in S1P-treated BMDMs. Endogenous ACOD1/itaconate in BMDMs suppressed BMDM proinflammatory activation by forming negative feedback with NF-κB signaling. S1P-regulated ACOD1 expression and BMDM activation via the same signaling pathway (S1PR2/MAPK/NF-κB signaling), indicating the endogenous brake function of ACOD1/itaconate. In chimeric mice with BM Acod1 deficiency, the abolition of the endogenous brake function of ACOD1/itaconate aggravated liver inflammation/fibrosis. Exclusive BM Acod1 expression showed the opposite effects.
conclusionsACOD1/itaconate exerts an endogenous brake function in the proinflammatory activation of BMDMs during chronic liver injury. Our data demonstrate the role of ACOD1/itaconate in S1P-induced BMDM activation, further indicating that ACOD1/itaconate is a potential therapeutic strategy for liver inflammation/fibrosis.
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