2018
DOI: 10.1016/j.diff.2017.12.001
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Mechanisms of epithelial thickening due to IL-1 signalling blockade and TNF-α administration differ during wound repair and regeneration

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Cited by 15 publications
(14 citation statements)
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“…Mescher's hypothesis relies on experimental studies in different models of regeneration: full-thickness injuries in fetal skin [126], transgenic mouse models deficient for specific immune cells [127], hind-limb amputation in urodeles and anurans [128]. The given evidence suggests that the profile of the infiltrated immune cells and their interactions within the injured tissue directly influences inflammation and scarring [125,129,130].…”
Section: Perspective On the Effect Of The Immune System In The Evolution Of Regenerative Capacitiesmentioning
confidence: 99%
“…Mescher's hypothesis relies on experimental studies in different models of regeneration: full-thickness injuries in fetal skin [126], transgenic mouse models deficient for specific immune cells [127], hind-limb amputation in urodeles and anurans [128]. The given evidence suggests that the profile of the infiltrated immune cells and their interactions within the injured tissue directly influences inflammation and scarring [125,129,130].…”
Section: Perspective On the Effect Of The Immune System In The Evolution Of Regenerative Capacitiesmentioning
confidence: 99%
“…IL‐1 family members are key inflammatory cytokines that generally act synergistically to amplify the inflammatory response. During wound healing, IL‐1 is expressed majorly by neutrophils and macrophages 48 …”
Section: Exudative Phase (Inflammatory/hemostasis Phase)mentioning
confidence: 99%
“…-1 family members are key inflammatory cytokines that generally act synergistically to amplify the inflammatory response.During wound healing, IL-1 is expressed majorly by neutrophils and macrophages 48. Decreased inflammatory cell numbers and reduced epidermal thickness and fibrosis are found in the IL-1R KO mice and wild-type mice treated with IL-1ra 49.…”
mentioning
confidence: 99%
“…This cytokine has two subtypes, IL-1a and IL-1b, and the latter is deeply involved in the pathogenesis of PTOA. [3][4][5] Recent studies have indicated that IL-1 levels in synoviocytes and in the medium supernatant of chondrocytes from patients with PTOA and in mouse models are significantly increased in in vitro experiments, and IL-1b is mainly responsible. 6,7 Attur et al have shown that IL-1b is related to the severity of joint pain and radiological findings in patients with PTOA.…”
Section: Proinflammatory Cytokines Includingmentioning
confidence: 99%