IFN-γ-mediated inhibition of JAK/STAT signaling via nano-scutellarin treatment is an efficient strategy for ameliorating liver fibrosis.

ABSTRACT:

Background

Metabolic dysfunction-associated steatohepatitis (MASH) is a large group of metabolic diseases that are hazardous to human health. Endothelial-to-mesenchymal transition (EndMT) mediated myofibroblast activation is an important factor that aggravates the development of liver fibrosis during MASH. However, the limited understanding of the underlying molecular mechanisms that drive EndMT in MASH has hindered the development of molecularly targeted therapies specifically targeting this pathological process.

Methods

We employed wild-type and ifn-γ-deficient mice, MASH models were induced repeated CCl₄ injections and a high-fat diet to verify the significance of IFN-γ role in vivo and its impact in EndMT. Male mice models of MASH were used to further analyze

SUBMITTER: Wang T 

PROVIDER: S-EPMC11834254 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature