2022
DOI: 10.1016/j.cytogfr.2022.03.001
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Scarless wound healing: Current insights from the perspectives of TGF-β, KGF-1, and KGF-2

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Cited by 59 publications
(31 citation statements)
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“…TGF-β is also important in protecting keratinocytes from oxidative stress and involves in the wound healing process [ 192 , 193 ]. The inhibition of TGF-β is demonstrated to accelerate wound closure and reduce scarring [ 194 , 195 ]. Exogenous SMAD7 below an oncogenic level can mitigate wound healing and skin inflammation defects related to over activation of TGF-β and NF-κB [ 196 ].…”
Section: The Function Of Tgf-β Signals In Diseasementioning
confidence: 99%
“…TGF-β is also important in protecting keratinocytes from oxidative stress and involves in the wound healing process [ 192 , 193 ]. The inhibition of TGF-β is demonstrated to accelerate wound closure and reduce scarring [ 194 , 195 ]. Exogenous SMAD7 below an oncogenic level can mitigate wound healing and skin inflammation defects related to over activation of TGF-β and NF-κB [ 196 ].…”
Section: The Function Of Tgf-β Signals In Diseasementioning
confidence: 99%
“…During the hemostasis phase, TGF-β released from blood platelets could recruit macrophages, T cells, and fibroblasts stimulating immune responses, angiogenesis, and collagen synthesis. VEGF is one of the growth factors induced by TGF-β and shows consistent results as TGF-β . Therefore, the PZBA–PVA hydrogel facilitated wound healing by triggering the expression of TGF-β and its growth factors such as VEGF and regulating inflammatory cytokines, including TNF-α and IL-1β .…”
Section: Resultsmentioning
confidence: 83%
“…TGF-β is mainly expressed by macrophages and plays a huge role in ECM repair. Insufficient TGF-β secretion is not conducive to the repair of ECM while excessive TGF-β secretion may cause fibrosis [ 17 ]. So under the condition of inflammation, the effect of scaffold on TGF-β secretion of macrophage at different time is studied.…”
Section: Resultsmentioning
confidence: 99%
“…Thus, promoting macrophages’ transformation from M1 to M2 phenotype is the dominant strategy to facilitate ECM remodeling and healthy tissue repair [ 15 , 16 ]. However, due to the release of cytokines, metabolites and growth factors and the clearance of debris with macrophages, and the recruitment of fibroblasts to migrate, proliferate and produce new ECM by macrophages [ 17 ]. The arbitrary inhibition of M1 macrophages and premature promotion of the M2 phenotype are associated with delayed wound healing, excessive ECM deposition, poorly formed neovascularization and pathological fibrosis [ 18 , 19 ].…”
Section: Introductionmentioning
confidence: 99%