Hepatospecific ablation of p38α MAPK governs liver regeneration through modulation of inflammatory response to CCl₄-induced acute injury.

ABSTRACT: Mammalian p38α MAPK (Mitogen-Activated Protein Kinase) transduces a variety of extracellular signals that regulate cellular processes, such as inflammation, differentiation, proliferation or apoptosis. In the liver, depending of the physiopathological context, p38α acts as a negative regulator of hepatocyte proliferation as well as a promotor of inflammatory processes. However, its function during an acute injury, in adult liver, remains uncharacterized. In this study, using mice that are deficient in p38α specifically in mature hepatocytes, we unexpectedly found that lack of p38α protected against acute injury induced by CCl₄ compound. We demonstrated that the hepatoprotective effect alleviated ROS accumulation and shaped the inflammatory response to promote efficient tissue re

SUBMITTER: Fortier M 

PROVIDER: S-EPMC6787013 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature