The orphan receptor GPRC5B promotes macrophage infiltration and an inflammatory plaque phenotype in atherosclerosis
Background and aims - Atherosclerosis is driven by chronic inflammation of the vascular wall, in which macrophages play a central role. The orphan G protein-coupled receptor GPRC5B is expressed in vascular cells and macrophages and is upregulated during monocyte-to-macrophage differentiation. It has...
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| Main Authors: | , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
January-February 2026
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| In: |
Cardiovascular pathology
Year: 2026, Volume: 80, Pages: 1-5 |
| ISSN: | 1879-1336 |
| DOI: | 10.1016/j.carpath.2025.107784 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.carpath.2025.107784 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S1054880725000699 
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| Author Notes: | Greta Verena Freundt, Friedrich Alexander von Samson-Himmelstjerna, Jan-Thorge Nitz, Frederik Stelter, Norbert Frey, Mark Luedde, Michael R. Preusch, Hans-Jörg Hippe |
| Summary: | Background and aims - Atherosclerosis is driven by chronic inflammation of the vascular wall, in which macrophages play a central role. The orphan G protein-coupled receptor GPRC5B is expressed in vascular cells and macrophages and is upregulated during monocyte-to-macrophage differentiation. It has been shown to activate NFκB-dependent inflammatory pathways in adipose tissue and glomeruli. Here, we investigated the impact of GPRC5B on macrophage infiltration and the progression of atherosclerotic plaque development in vivo. - Methods - Bone marrow from heterozygous GPRC5B-transgenic C57BL/6 mice and wild-type controls was transplanted into lethally irradiated LDL receptor-deficient mice. Animals were fed a Western-type diet for 16 weeks, after which atherosclerotic lesions in the aortic sinus were analyzed. - Results - Mice receiving GPRC5B-transgenic bone marrow showed no significant differences in serum lipids or cardiac mass indices. However, they exhibited significantly increased macrophage infiltration within atherosclerotic plaques and a non-significant trend toward larger and more complex lesions. - Conclusions - GPRC5B overexpression in bone marrow-derived monocyte/macrophage lineage cells promotes a more inflammatory plaque phenotype, characterized by enhanced macrophage infiltration. These findings highlight GPRC5B as a potential modulator of plaque progression and suggest it may represent a novel therapeutic target in vascular inflammation and atherosclerosis. |
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| Item Description: | Online verfügbar: 1. Oktober 2025, Artikelversion: 7. Oktober 2025 Gesehen am 23.03.2026 |
| Physical Description: | Online Resource |
| ISSN: | 1879-1336 |
| DOI: | 10.1016/j.carpath.2025.107784 |