PP1A prevents ROS‐induced pyroptosis by inhibiting MAPK/caspase‐3 in mouse adipose tissue

Abstract

Pyroptosis is a type of programmed cell death triggered by a variety of exogenous stimuli, playing important roles in the development of cells. Recent studies have shown that pyroptosis also occurs in human and mouse adipocytes. The serine/threonine protein phosphatase 1 catalytic subunit α (PP1A) is located in the nucleus and functions in the regulation of cell development, glucose metabolism and protein synthesis. PP1A can also target important proteins in the process of apoptosis. However, it is still unclear whether PP1A participates in the regulation of pyroptosis in mouse adipocytes. In the present study, we investigated the function of PP1A in reactive oxygen species‐induced pyroptosis and the related mechanism in mouse adipose tissue. Our results demonstrated that PP1A suppressed pyroptosis in adipocytes by inhibiting the reactive oxygen species/mitogen‐activated protein kinase/caspase‐3 signaling pathway and promoting M2 macrophage polarization. This experiment provides a theoretical basis for understanding the regulatory function and mechanism of PP1A in pyroptosis caused by oxidative stress in adipocytes.

Macrophage Perspectives in Liver Diseases: Programmed Death, Related Biomarkers, and Targeted Therapy

“…Conversely, IL-4 and IL-13 induce M2 polarization, which promotes anti-inflammatory processes and tissue repair. The susceptibility of macrophages to various forms of PCD can be influenced by their polarization status, the level of microenvironmental inflammation, and the presence of ROS and peroxides [ 39 , 40 ]. While macrophage autophagy often promotes M1 polarization, leading to chronic inflammation and liver damage in obese mice, the vulnerability of these M1 macrophages to specific PCD pathways varies [ 41 ].…”