GPR18 and inflammatory response: For DRV2/GPR18, convergent evidence across hematopoietic and CV models indicates that RvD2–GPR18 activation reprograms innate immunity and limits adverse remodeling: in pressure-overload heart failure, the RvD2/GPR18 axis improves function and attenuates Ly6Chigh macrophage polarization via STAT1 and NF-κB p65 pathways, with genetic loss of GPR18 abolishing benefit [135]; in abdominal aortic aneurysm, RvD2/GPR18 signaling enhances monocytic MDSC function, reduces vascular inflammation, and mitigates structural degeneration [136].