ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
GPR132 antagonists alleviate atherosclerosis by suppressing M1 polarization and subsequent VSMCs proliferation and migration as revealed by transcriptomic profiling.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAtherosclerosis (AS) is a chronic inflammatory disorder with substantial global prevalence, wherein macrophage polarization and vascular smooth muscle cells (VSMCs) phenotypic switching are critical pathogenic events. Although G protein-coupled receptor 132 (GPR132) is markedly expressed in macrophages, its specific role and mechanism in AS-associated macrophage polarization remain incompletely understood.
methodsPharmacological antagonism of GPR132 was evaluated in high-fat diet-fed ApoE
resultsGPR132 antagonism attenuated atherosclerotic lesion progression and reduced pro‑inflammatory cytokine secretion without altering lipid profiles. GPR132 was enriched in pro‑inflammatory (M1‑like) macrophage subpopulations within plaques, which also upregulated VSMC‑promoting growth factors. GPR132 overexpression promoted M1 macrophage polarization and suppressed IL‑4‑induced M2 macrophage polarization, whereas knockout enhanced M2 and attenuated M1. Conditioned medium from GPR132‑overexpressing macrophages significantly enhanced VSMCs proliferation and migration. Mechanistically, GPR132 drove M1 macrophage polarization primarily through activation of the p38/MAPK signaling pathway, an effect reversible by SB203580 or GPR132 antagonists.
conclusionsGPR132 promotes pro‑inflammatory macrophage polarization via p38/MAPK signaling, and its antagonism mitigates atherosclerotic progression by suppressing inflammatory microenvironments and VSMCs proliferation/migration, highlighting GPR132 as a potential therapeutic target for AS.
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