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Eming, S. A., Wynn, T. A., & Martin, P. (2017). Inflammation and metabolism in tissue repair and regeneration. Science, 356(6342), 1026–1030. Added by: Dr. Enrique Feoli (26/04/2023, 19:59) Last edited by: Dr. Enrique Feoli (26/04/2023, 20:09) |
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| Resource type: Journal Article DOI: 10.1126/science.aam7928 BibTeX citation key: Eming2017 View all bibliographic details  |
Categories: BioAcyl Corp, BioAcyl Corp Subcategories: Scar complications, Wound Healing Creators: Eming, Martin, Wynn Collection: Science |
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| Abstract |
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Tissue repair after injury is a complex, metabolically demanding process. Depending on the tissue’s regenerative capacity and the quality of the inflammatory response, the outcome is generally imperfect, with some degree of fibrosis, which is defined by aberrant accumulation of collagenous connective tissue. Inflammatory cells multitask at the wound site by facilitating wound debridement and producing chemokines, metabolites, and growth factors. If this well-orchestrated response becomes dysregulated, the wound can become chronic or progressively fibrotic, with both outcomes impairing tissue function, which can ultimately lead to organ failure and death. Here we review the current understanding of the role of inflammation and cell metabolism in tissue-regenerative responses, highlight emerging concepts that may expand therapeutic perspectives, and briefly discuss where important knowledge gaps remain.
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| Notes |
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HIF-1α activation and glycolysis are hallmarks of inflammatory activation. In contrast, mitochondrial biogenesis, FA degradation, an intact TCA cycle, and oxidative phosphorylation lead to efficient production of large amounts of ATP that sustain the secretory and resolution phenotype of type 2–activated macrophages. How the dynamics of macrophage polarization phenotypes (marker genes are depicted in triangles in the middle panel) and cellular metabolic pathways instruct the sequence of specific repair mechanisms at a tissue level remains undetermined. NADPH, nicotinamide adenine dinucleotide; e–, electron; PPP, pentose phosphate pathway; PRR, pathogen recognition receptor; PAMP, pathogen-associated molecular pattern; DAMP, damage-associated molecular pattern; TCA, tricarboxylic acid; SDH, succinate dehydrogenase; TAG, triacylglycerol; FFA, free fatty acids; LDL, low-density lipoprotein; VLDL, very-low-density lipoprotein.GRAPHIC: ADAPTED BY N. CARY/SCIENCE |
