Mitochondrial antiviral signaling protein enhances MASLD progression through the ERK/TNFα/NFκβ pathway.

ABSTRACT:

Background and aims

Mitochondrial antiviral signaling protein (MAVS) is a critical regulator that activates the host's innate immunity against RNA viruses, and its signaling pathway has been linked to the secretion of proinflammatory cytokines. However, the actions of MAVS on inflammatory pathways during the development of metabolic dysfunction-associated steatotic liver disease (MASLD) have been little studied.

Approach and results

Liver proteomic analysis of mice with genetically manipulated hepatic p63, a transcription factor that induces liver steatosis, revealed MAVS as a target downstream of p63. MAVS was thus further evaluated in liver samples from patients and in animal models with MASLD. Genetic inhibition of MAVS was performed in hepatocyte cell lines, primary hepa

SUBMITTER: Novoa E 

PROVIDER: S-EPMC11999095 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature