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[瘢痕疙瘩(第一部分):临床表现、流行病学、组织学及发病机制]

[Keloid scars (part I): Clinical presentation, epidemiology, histology and pathogenesis].

作者信息

Philandrianos C, Kerfant N, Jaloux C, Martinet L, Bertrand B, Casanova D

机构信息

Service de chirurgie plastique et réparatrice, hôpital Nord, AP-HM, CHU de Marseille, chemin des Bourrely, 13915 Marseille cedex 20, France.

Service de chirurgie plastique, CHRU La Cavale Blanche, boulevard Tanguy-Prigent, 29609 Brest, France.

出版信息

Ann Chir Plast Esthet. 2016 Apr;61(2):128-35. doi: 10.1016/j.anplas.2015.09.005. Epub 2015 Nov 3.

DOI:10.1016/j.anplas.2015.09.005
PMID:26545809
Abstract

Keloid scars are a dysregulated response to cutaneous wound healing and are characterized by excessive deposition of collagen. Clinical and histological aspects are typical but they are often confused with hypertrophic scars. Principal pathogenesis is abnormal regulation of the collagen equilibrium because of TGFβ. In this first part, clinical characteristics, physiopathology and histology of keloid scars are explained.

摘要

瘢痕疙瘩是皮肤伤口愈合的一种失调反应,其特征是胶原蛋白过度沉积。临床和组织学方面具有典型性,但它们常与增生性瘢痕相混淆。主要发病机制是由于转化生长因子β导致胶原蛋白平衡的异常调节。在第一部分中,将对瘢痕疙瘩的临床特征、生理病理学和组织学进行解释。

相似文献

1
[Keloid scars (part I): Clinical presentation, epidemiology, histology and pathogenesis].[瘢痕疙瘩(第一部分):临床表现、流行病学、组织学及发病机制]
Ann Chir Plast Esthet. 2016 Apr;61(2):128-35. doi: 10.1016/j.anplas.2015.09.005. Epub 2015 Nov 3.
2
Upregulation of the Wnt/beta-catenin pathway induced by transforming growth factor-beta in hypertrophic scars and keloids.转化生长因子-β诱导的肥厚性瘢痕和瘢痕疙瘩中Wnt/β-连环蛋白信号通路的上调
Acta Derm Venereol. 2006;86(4):300-7. doi: 10.2340/00015555-0101.
3
Studies of transforming growth factors beta 1-3 and their receptors I and II in fibroblast of keloids and hypertrophic scars.瘢痕疙瘩和增生性瘢痕成纤维细胞中转化生长因子β1-3及其Ⅰ型和Ⅱ型受体的研究
Acta Derm Venereol. 2005;85(3):216-20. doi: 10.1080/00015550410025453.
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Conditioned medium from keloid keratinocyte/keloid fibroblast coculture induces contraction of fibroblast-populated collagen lattices.瘢痕疙瘩角质形成细胞/瘢痕疙瘩成纤维细胞共培养的条件培养基可诱导成纤维细胞填充的胶原晶格收缩。
Br J Dermatol. 2005 Apr;152(4):639-45. doi: 10.1111/j.1365-2133.2005.06545.x.
5
mTOR as a potential therapeutic target for treatment of keloids and excessive scars.雷帕霉素靶蛋白作为治疗瘢痕疙瘩和增生性瘢痕的潜在治疗靶点。
Exp Dermatol. 2007 May;16(5):394-404. doi: 10.1111/j.1600-0625.2007.00550.x.
6
Smad interacting protein 1 as a regulator of skin fibrosis in pathological scars.Smad 相互作用蛋白 1 作为病理性瘢痕皮肤纤维化的调节剂。
Burns. 2011 Jun;37(4):665-72. doi: 10.1016/j.burns.2010.12.001. Epub 2011 Jan 14.
7
[Keloid scars: a case series study].[瘢痕疙瘩:病例系列研究]
Ann Pathol. 2015 Apr;35(2):148-53. doi: 10.1016/j.annpat.2014.10.007. Epub 2015 Feb 14.
8
A novel truncated TGF-beta receptor II downregulates collagen synthesis and TGF-beta I secretion of keloid fibroblasts.一种新型截短的转化生长因子β受体II可下调瘢痕疙瘩成纤维细胞的胶原蛋白合成及转化生长因子βI分泌。
Connect Tissue Res. 2008;49(2):92-8. doi: 10.1080/03008200801913924.
9
Asiaticoside suppresses collagen expression and TGF-β/Smad signaling through inducing Smad7 and inhibiting TGF-βRI and TGF-βRII in keloid fibroblasts.积雪草苷通过诱导 Smad7 并抑制瘢痕成纤维细胞中的 TGF-βRI 和 TGF-βRII 来抑制胶原表达和 TGF-β/Smad 信号通路。
Arch Dermatol Res. 2011 Oct;303(8):563-72. doi: 10.1007/s00403-010-1114-8. Epub 2011 Jan 15.
10
Morphological and immunochemical differences between keloid and hypertrophic scar.瘢痕疙瘩与增生性瘢痕之间的形态学和免疫化学差异。
Am J Pathol. 1994 Jul;145(1):105-13.

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Mol Med Rep. 2021 Jan;23(1). doi: 10.3892/mmr.2020.11693. Epub 2020 Nov 17.
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Near-infrared-emitting nanoparticles activate collagen synthesis via TGFβ signaling.近红外发光纳米颗粒通过 TGFβ 信号通路激活胶原蛋白合成。
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FoxO3a depletion accelerates cutaneous wound healing by regulating epithelial‑mesenchymal transition through β‑catenin activation.FoxO3a 缺失通过激活 β-连环蛋白调控上皮-间充质转化加速皮肤伤口愈合。
Mol Med Rep. 2020 Mar;21(3):1224-1232. doi: 10.3892/mmr.2020.10912. Epub 2020 Jan 3.
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