What Is the Impact of Depletion of Immunoregulatory Genes on Wound Healing? A Systematic Review of Preclinical Evidence

Figure 6

Location of the molecules of depleted genes addressed in this review and their participation in metabolic pathways involved in the wound repair. The effect of depleted genes on wound closure was shown by the colors: red (delayed), green (accelerated), and yellow (unchanged). PM: plasma membrane; ECM: extracellular matrix; 5-LO: 5-Lipoxygenase; α-kl: alpha-Klotho; bFGF: basic Fibroblastic Growth Factor; Cx43: Connexin 43; GM-CSF: Granulocyte-Macrophage Colony-Stimulating Factor; HO-2: Heme Oxygenase 2; ICOS: Inducible Costimulator; ICOSL: Inducible Costimulator Ligand; IFN-γ: Interferon-gamma; (IL-10, IL-6): Interleukins; KGF: Keratinocyte Growth Factor; Lum: Lumican; (MMP8, MMP9, MMP13, MMP14): Matrix Metalloproteinase; MK2: Mitogen-Activated Protein Kinase-2; Mstn: Myostatin; Nramp: Natural resistance-associated macrophage proteins; P311: Neuronal protein 3.1; Prdx6: Peroxiredoxin 6; Akt1: Serine/threonine kinase; (TPS1, TPS2): Thrombospondin; Nrf2: Transcription factor NF-E2-related factor 2; c-Myb: Transcription factor proto-oncogene c-Myb. Signaling pathways: Activin R: Activin Receptor; FGF R: Fibroblast Growth Factor Receptor; EGF R: Epidermal Growth Factor Receptor; TGF-β R: Transforming Growth Factor-β Receptor; NFE2L2/Nrf2: Nuclear Factor, Erythroid 2 Like 2; JNK: c-Jun N-terminal kinase; IFN-γ: Interferon-gamma; JAK/STAT: Janus Kinase Signal Transducer and Activator of Transcription.