Targeted inhibitors of S100A9 alleviate chronic pancreatitis by inhibiting M2 macrophage polarization via the TAOK3-JNK signaling pathway.

ABSTRACT:

Background

Chronic pancreatitis (CP) is a fibro-inflammatory syndrome with unclear pathogenesis and futile therapy. CP's microenvironment disrupts the fine-tuned balance of macrophage polarization toward a predominance of the M2-like phenotype associated with fibrosis. S100A9 is mainly expressed in monocytes as a potent regulator of macrophage phenotype and function. Here, we investigated the S100A9-related mechanisms underlying CP pathology induced by macrophages polarization.

Methods

S100a9 knockout (S100a9 _-/-) mice and an in vitro coculture system of macrophages overexpressing S100a9 and primary PSCs were constructed to investigate the effects and mechanisms of S100A9-mediated macrophage polarization on pancreatic inflammation and f

SUBMITTER: Tao X 

PROVIDER: S-EPMC11979270 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature