PPARs/macrophages: A bridge between the inflammatory response and lipid metabolism in autoimmune diseases

Abstract

Autoimmune diseases (AIDs) are a collection of pathologies that arise from autoimmune reactions and lead to the destruction and damage of the body's tissues and cellular components, ultimately resulting in tissue damage and organ dysfunction. The anti-inflammatory effects of the peroxisome proliferator-activated receptor (PPAR), a pivotal regulator of lipid metabolism, are crucial in the context of AIDs. PPAR mitigates AIDs by modulating macrophage polarization and suppressing the inflammatory response. Numerous studies have demonstrated the crucial involvement of lipid metabolism and phenotypic switching in classically activated (M1)/alternatively activated (M2)-like macrophages in the inflammatory pathway of AIDs. However, the precise mechanism by which PPAR, a critical mediator between of lipid metabolism and macrophage polarization, regulates macrophage polarization remains unclear. This review aimed to clarify the role of PPAR and macrophages in the triangular relationship among AIDs, lipid metabolism, and inflammatory response, and aims to summarize the mechanism of the PPAR-mediated macrophage activation and polarization, which impacts the progression and development of AIDs.