Resolvine

Resolvine, a term sometimes used to refer to resolvins in the scientific literature, denotes a set of specialized pro-resolving lipid mediators involved in the active termination of inflammation. Resolvin nomenclature is typically divided into two main series derived from omega-3 fatty acids: E-series resolvins (RvE) from eicosapentaenoic acid (EPA) and D-series resolvins (RvD) from docosahexaenoic acid (DHA).

Biosynthesis and origin occur in inflamed or injured tissues and in circulating leukocytes. Enzymatic oxygenation by cyclooxygenases and lipoxygenases converts EPA and DHA into intermediate hydroxy products that are further processed into active resolvins. In the presence of aspirin, acetylated COX-2 can initiate certain pathways, notably for some RvE1 production. Resolvin formation is part of a broader program of lipid mediators that promote the resolution phase of inflammation.

Mechanisms of action involve signaling through specific G-protein-coupled receptors and downstream pathways that reduce neutrophil recruitment, enhance macrophage clearance of apoptotic cells, and suppress pro-inflammatory mediator production. Receptor interactions vary by resolvin subtype; for example, some resolvins engage receptors such as ChemR23 and ALX/FPR2, among others, to trigger pro-resolving cellular responses.

Biological roles encompass contributions to tissue homeostasis and host defense during and after inflammatory challenges. Endogenous resolvines are detected in plasma, tissues, and biological fluids at low concentrations, and their production is associated with efficient resolution; altered metabolism or deficiency has been examined in various disease models.

Research status and applications remain exploratory. No resolvin-based therapies are approved, but preclinical studies investigate synthetic analogs and stable formulations to harness pro-resolving actions in inflammatory and metabolic disorders. See also specialized pro-resolving mediators, omega-3 fatty acids, and inflammation resolution.