ArticlePhysiological reports2026
Conditional ablation of RGS2 in myeloid cells does not influence blood pressure and organ damage in angiotensin II-induced hypertension in mice.
Article in Physiological reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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15 authors.
Funding
Abstract
The role of the immune system in the development of hypertension is well-established. Recent studies revealed the critical role of G-protein-coupled receptor signaling, particularly angiotensin II (Ang II) type 1 receptor (AT1R), in immune cell function. Regulator of G-protein signaling (RGS) proteins are critical players in terminating G-protein-coupled receptor signaling, with RGS2 being particularly interesting because it limits signaling downstream of AT1R. Importantly, RGS2 is highly expressed in myeloid immune cells. Global RGS2 deletion results in elevated blood pressure and Ang II-dependent vascular hypercontractility. While evidence supports a key role for RGS2 in vascular tissue, its role in immune cells remains underexplored. Herein, we hypothesized that genetic ablation of RGS2 in myeloid cells would amplify Ang II signaling, thereby exacerbating the inflammatory response to Ang II. To test this hypothesis, we employed a conditional myeloid-specific RGS2 knockout mouse model (RGS2
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