Xing-Guo Li1,2,3,#, Lu-Kai Wang4,#, Fu-Ming Tsai5, Hsueh-Chun Wang1,*
BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.075492
- 09 June 2026
Abstract Itaconate, produced by aconitate decarboxylase 1 (ACOD1, also known as IRG1), acts as a key immunometabolite that inhibits succinate dehydrogenase (SDH) and can engage reduction-oxidation (redox)-sensitive signaling programs. This review summarizes the emerging, context-dependent roles of the ACOD1-itaconate axis in cancer, while critically distinguishing between the effects of endogenous itaconate and its cell-permeable derivatives. In tumor cells, endogenous ACOD1 expression or uptake via solute carrier family 13 member 3 (SLC13A3) alters oxidative phosphorylation and glycolysis. In the tumor microenvironment, myeloid-derived itaconate contributes to immune tolerance by reducing dendritic-cell cross-priming and limiting CD8+ T-cell metabolic activity. Moreover, More >