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Effects of Acod1 loss on liver responses to fat overnutrition

ABSTRACT: ACOD1 is the enzyme repurposing cisaconitate from the tricarboxylic acid (TCA) cycle in the mitochondria to produce itaconate, a metabolite with anti-inflammatory and tolerogenic functions. In particular, itaconate accumulation in macrophages is known to oppose pro-inflammatory cytokine production mainly by inhibiting succinate dehydrogenase activity, activating the NRF2 and ATF3driven responses and inhibiting NLRP3. Itaconate biosynthesis was found to be induced in the liver of mice exposed to ischemia reperfusion (I/R) stress and to oppose the resulting tissue injury by sustaining hepatoprotective antioxidant programs. Whether ACOD1 plays a role in the homeostatic response of liver to different noninfectious injuring conditions remains largely unexplored. This study investigates the contribution of itaconate biosynthesis in the response of liver to dietary lipid overload and in the development of associated nonalcoholic fatty liver disease.

INSTRUMENT(S): Bruker timsTOF Pro

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Simone Cardaci

PROVIDER: MSV000090276 | MassIVE |

REPOSITORIES: MassIVE

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