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From lipid switch to tissue repair: how resolvins reprogram macrophage polarization and function

From lipid switch to tissue repair: how resolvins reprogram macrophage polarization and function

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DOI	10.1097/IN9.0000000000000076
刊名	Immunometabolism IJ
年，卷(期)	2026, 8(1)
作者	Buete, Rebecca; Scherer, Jordan; Patsalos, Andreas; Nagy, Laszlo,
作者单位	Johns Hopkins Univ, Johns Hopkins All Childrens Hosp JHACH, Inst Fundamental Biomed Res, Dept Med,Sch Med, St Petersburg, FL 21218 USA;
摘要	Specialized pro-resolving mediators (SPMs) derived from docosahexaenoic acid (DHA), particularly D-series resolvins (RvD1, RvD2, RvD3, and RvD5), function to terminate inflammation while preserving host defense. They are synthesized from DHA by lipoxygenases and act through G-protein-coupled receptors and lipid-sensing transcription factors (TFs). These mediators reprogram macrophage metabolism towards fatty-acid oxidation and oxidative phosphorylation, accelerate efferocytosis, and promote tissue repair. Here, we synthesize current knowledge on their biosynthesis, receptor signaling, and immunometabolic rewiring within macrophages, and critically appraise their therapeutic potential across cardiometabolic, musculoskeletal, autoimmune, and ischemia/reperfusion disorders. We also discuss analytical controversies surrounding their in vivo low-abundance detection, and outline translational challenges including short half-life, formulation stability, and emerging synthetic agonists. Finally, we propose priority research directions, from single-cell spatial lipidomics to clinical translation, to define the next frontier for resolvin-based immunotherapies.
Abstract	Specialized pro-resolving mediators (SPMs) derived from docosahexaenoic acid (DHA), particularly D-series resolvins (RvD1, RvD2, RvD3, and RvD5), function to terminate inflammation while preserving host defense. They are synthesized from DHA by lipoxygenases and act through G-protein-coupled receptors and lipid-sensing transcription factors (TFs). These mediators reprogram macrophage metabolism towards fatty-acid oxidation and oxidative phosphorylation, accelerate efferocytosis, and promote tissue repair. Here, we synthesize current knowledge on their biosynthesis, receptor signaling, and immunometabolic rewiring within macrophages, and critically appraise their therapeutic potential across cardiometabolic, musculoskeletal, autoimmune, and ischemia/reperfusion disorders. We also discuss analytical controversies surrounding their in vivo low-abundance detection, and outline translational challenges including short half-life, formulation stability, and emerging synthetic agonists. Finally, we propose priority research directions, from single-cell spatial lipidomics to clinical translation, to define the next frontier for resolvin-based immunotherapies.
关键词	specialized pro-resolving mediators; d-series resolvins; resolution of inflammation; macrophage; macrophage signaling; macrophage polarization; metabolic disease; immunomodulation; atherosclerosis; diabetes mellitus; rheumatoid arthritis; duchenne muscular dystrophy
KeyWord	specialized pro-resolving mediators; d-series resolvins; resolution of inflammation; macrophage; macrophage signaling; macrophage polarization; metabolic disease; immunomodulation; atherosclerosis; diabetes mellitus; rheumatoid arthritis; duchenne muscular dystrophy
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引用本文

Buete, Rebecca; Scherer, Jordan; Patsalos, Andreas; Nagy, Laszlo. From lipid switch to tissue repair: how resolvins reprogram macrophage polarization and function [J]. Immunometabolism. 2026; 8; (1). - .

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