Wang Zikang, Wang Miao, Xu Xiaoyu, Liu Yunyan, Chen Qian, Wu Bin, Zhang Ying
College of Traditional Chinese Medicine, Chongqing Medical University, Chongqing, 401334, China.
Department of Rheumatology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, 400021, China.
Biochem Biophys Res Commun. 2023 Oct 17;684:149128. doi: 10.1016/j.bbrc.2023.149128.
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.
自身免疫性疾病(AIDs)是一类由自身免疫反应引发的病理状况,会导致身体组织和细胞成分的破坏与损伤,最终造成组织损伤和器官功能障碍。过氧化物酶体增殖物激活受体(PPAR)作为脂质代谢的关键调节因子,其抗炎作用在自身免疫性疾病中至关重要。PPAR通过调节巨噬细胞极化和抑制炎症反应来减轻自身免疫性疾病。众多研究表明,脂质代谢和经典激活(M1)/替代激活(M2)样巨噬细胞的表型转换在自身免疫性疾病的炎症途径中起着关键作用。然而,PPAR作为脂质代谢与巨噬细胞极化之间的关键介质,调节巨噬细胞极化的确切机制仍不清楚。本综述旨在阐明PPAR和巨噬细胞在自身免疫性疾病、脂质代谢和炎症反应三角关系中的作用,并总结PPAR介导的巨噬细胞激活和极化机制,该机制影响自身免疫性疾病的进展和发展。