Resolvin (Rv)

Resolvins are a family of endogenous lipid mediators derived from omega-3 fatty acids (EPA, DHA, n-3 DPA) that play a central role in actively resolving inflammation and restoring tissue homeostasis[1][3][5]. Formed by enzymatic pathways involving lipoxygenases, cyclooxygenases, and cytochrome P450, resolvins bind and activate specific GPCRs, triggering anti-inflammatory and pro-resolving mechanisms via reduced leukocyte infiltration, enhanced phagocytosis of cellular debris, and suppression of pro-inflammatory mediator production[4][5][7]. Multiple resolvin species (e.g., RvD1, RvD2, RvE1) exert disease-modifying effects in cancer, cardiovascular, neurodegenerative, metabolic, and inflammatory diseases, with promising but as-yet-unproven efficacy and safety in clinical settings[2][4][6][8]. Their clinical potential as therapeutics lies in mimicking or enhancing the body's natural resolution pathways without the immunosuppression or toxicity seen with conventional anti-inflammatory agents[2][8].

Other names

Specialized pro-resolving mediators (SPM)SPMsPro-resolving lipid mediatorsD-series resolvin (RvD1, RvD2)E-series resolvin (RvE1, RvE2, RvE3)RvT series (13-series resolvins)Protectins, maresins, and lipoxins are related but distinct families

Activation of specific G protein-coupled receptors (GPCRs), notably ALX/FPR2 (RvD1), ChemR23 (RvE1), GPR32 (RvD1), and BLT-1 antagonism (RvE1 and RvE2). Downregulation of NF-κB and MAPK signaling pathways. Suppression of pro-inflammatory cytokines (e.g., TNF-α, IL-6, IL-1β). Induction of apoptosis in neutrophils and promotion of macrophage-mediated clearance. Inhibition of platelet activation and leukocyte adhesion. Augmentation of antioxidant defense (e.g., SOD, HO-1).