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Res."],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Atherosclerosis (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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Pharmacological antagonism of GPR132 was evaluated in high-fat diet-fed ApoE\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. Integrated single-cell RNA sequencing and transcriptome analyses from GEO datasets were performed to profile GPR132 expression in murine and human atherosclerotic plaques. In vitro, GPR132 overexpression and knockout macrophages were generated to assess M1\/M2 polarization markers, and an indirect co\u2011culture system with VSMCs was established. Mechanistic investigations employed RNA\u2011sequencing and Western blotting, with pathway inhibition using SB203580 or GPR132 antagonists.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>GPR132 antagonism attenuated atherosclerotic lesion progression and reduced pro\u2011inflammatory cytokine secretion without altering lipid profiles. GPR132 was enriched in pro\u2011inflammatory (M1\u2011like) macrophage subpopulations within plaques, which also upregulated VSMC\u2011promoting growth factors. GPR132 overexpression promoted M1 macrophage polarization and suppressed IL\u20114\u2011induced M2 macrophage polarization, whereas knockout enhanced M2 and attenuated M1. Conditioned medium from GPR132\u2011overexpressing 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>GPR132 promotes pro\u2011inflammatory 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00011-026-02342-2","type":"journal-article","created":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:00:58Z","timestamp":1787022058000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["GPR132 antagonists alleviate atherosclerosis by suppressing M1 polarization and subsequent VSMCs proliferation and migration as revealed by transcriptomic profiling"],"prefix":"10.1007","volume":"75","author":[{"given":"Yin","family":"Feng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zheng","family":"Cao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinwei","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lilliane","family":"Aol","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liqun","family":"He","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,8,18]]},"reference":[{"key":"2342_CR1","doi-asserted-by":"publisher","first-page":"191","DOI":"10.1146\/annurev-med-042418-011108","volume":"71","author":"IJ Goldberg","year":"2020","unstructured":"Goldberg IJ, Sharma G, Fisher EA. 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