ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Endothelial GPR68 Is Essential for Arteriogenesis and Represents a Therapeutic Target in a Model of Peripheral Artery Disease.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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
Peripheral artery disease (PAD) is characterized by arterial narrowing that reduces limb perfusion, causing significant morbidity. The body can compensate via shear stress-driven collateral artery growth (arteriogenesis). However, the primary receptors of mechanical forces on the endothelial cells in PAD remain poorly defined. Human phenome‑wide association study (PheWAS) shows that variants near GPR68, a gene encoding shear-stress sensitive G protein-coupled receptor (GPCR), are associated with increased PAD risk. To investigate the role of GPR68 in arteriogenesis in PAD, hindlimb ischemia (HLI) was employed in inducible, endothelial cell-specific Gpr68 knockout mice (Gpr68 iECKO) as well as littermate controls. Impaired blood perfusion recovery, smaller collateral artery diameter, and exacerbated distal muscle injury were observed in Gpr68 iECKO. Mechanistically, these defects were associated with a reduction in perivascular CCR2
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