Parkin deficiency aggravates inflammation-induced acute lung injury by promoting necroptosis in alveolar type II cells.

ABSTRACT:

Background

Necroptosis is a form of programmed cell death resulting in tissue inflammation due to the release of intracellular contents. Its role and regulatory mechanism in the context of acute lung injury (ALI) are unclear. Parkin (Prkn), an E3 ubiquitin ligase, has recently been implicated in the regulation of necroptosis. In this study, we aimed to investigate the role and mechanism of Parkin in the process of ALI.

Methods

Lipopolysaccharides (LPS)-induced mouse ALI model was utilized, and the pathological changes in lung tissues were characterized. To elucidate the roles of Parkin and necroptosis in this context, mixed lineage kinase domain-like (Mlkl) knockout mice, Prkn conditional knockout mice, and the necroptosis inhibitor were employed. Additionally,

SUBMITTER: Quan M 

PROVIDER: S-EPMC11742354 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature