Immunometabolic regulation of tissue repair: a conceptual framework (IMAGE)
Caption
Tissue injury triggers a dynamic repair niche that is coordinated by metabolic stress, inflammatory and danger signals, and structural or stromal cues. Within this niche, immune cells undergo metabolic adaptation to accommodate local environmental changes and stage-specific repair demands. These adaptive metabolic programs instruct immune effector and repair-associated functions, including host defense, debris clearance, efferocytosis, inflammation resolution, mediator production, angiogenesis, and support for tissue progenitors. Conversely, immune cells can also reshape the local repair niche through metabolite release and their interactions with stromal and epithelial compartments. Balanced immunometabolic regulation promotes regenerative repair and functional recovery, whereas persistent, excessive, or temporally mismatched metabolic activation may drive maladaptive outcomes, such as chronic inflammation, defective clearance, pathological fibrosis or scarring, and long-term tissue dysfunction. Abbreviations: ROS, reactive oxygen species; DAMPs, damage-associated molecular patterns; PAMPs, pathogen-associated molecular patterns; ECM, extracellular matrix; OXPHOS, oxidative phosphorylation; FAO, fatty acid oxidation; AA metabolism, amino acid metabolism; NETs, neutrophil extracellular traps. This figure was created using BioRender (https:// biore nder. com/)
Credit
Professor Di Wang from Zhejiang University, China; Dr. Zheyu Chi from Zhejiang University, China Image source link: https://link.springer.com/article/10.1007/s44466-026-00052-2
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