Gas6 induces AIM to suppress acute lung injury in mice by inhibiting NLRP3 inflammasome activation and inducing autophagy.

ABSTRACT:

Introduction

Growth arrest-specific 6 (Gas6) protein signaling plays a critical role in maintaining immune homeostasis and regulating inflammation. However, novel mechanisms for modulating macrophage activity through the Gas6 axis are being identified. Gas6 enhances the production of apoptosis inhibitor of macrophages (AIM), a protein with potent anti-inflammatory properties. This study investigates whether Gas6-induced AIM suppresses acute lung injury (ALI) in mice by modulating key inflammatory pathways, including inflammasome activation, autophagy, reactive oxygen species (ROS) generation, and efferocytosis.

Methods

ALI was induced in wild-type (WT) and AIM^-/- mice via intratracheal administration of LPS. To evaluate the effects of the Gas6-AIM axis on l

SUBMITTER: Jeong S 

PROVIDER: S-EPMC11873840 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature