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瘢痕疙瘩:皮肤纤维化的范例——发病机制与治疗

Keloids: The paradigm of skin fibrosis - Pathomechanisms and treatment.

作者信息

Andrews Jonathan P, Marttala Jaana, Macarak Edward, Rosenbloom Joel, Uitto Jouni

机构信息

Department of Dermatology and Cutaneous Biology, The Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.

Department of Dermatology and Cutaneous Biology, The Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA; The Joan and Joel Rosenbloom Research Center for Fibrotic Diseases, Thomas Jefferson University, Philadelphia, PA, USA.

出版信息

Matrix Biol. 2016 Apr;51:37-46. doi: 10.1016/j.matbio.2016.01.013. Epub 2016 Feb 2.

DOI:10.1016/j.matbio.2016.01.013
PMID:26844756
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4842154/
Abstract

Keloids, fibroproliferative dermal tumors with effusive accumulation of extracellular matrix (ECM) components, particularly collagen, result from excessive expression of growth factors and cytokines. The etiology of keloids is unknown but they occur after dermal injury in genetically susceptible individuals, and they cause both physical and psychological distress for the affected individuals. Several treatment methods for keloids exist, including the combination therapy of surgical excision followed by intralesional steroid therapy, however, they have high recurrence rate regardless of the current treatment method. Improved understanding of the pathomechanisms leading to keloid formation will hopefully identify pathways that serve as specific targets to improve therapy for this devastating, currently intractable, disorder.

摘要

瘢痕疙瘩是一种纤维增生性皮肤肿瘤,伴有细胞外基质(ECM)成分,特别是胶原蛋白的大量积聚,由生长因子和细胞因子的过度表达引起。瘢痕疙瘩的病因尚不清楚,但在遗传易感个体的皮肤损伤后会出现,给受影响的个体带来身体和心理上的痛苦。目前有几种治疗瘢痕疙瘩的方法,包括手术切除后病灶内注射类固醇的联合治疗,然而,无论采用何种治疗方法,其复发率都很高。更好地理解导致瘢痕疙瘩形成的发病机制有望找到可作为特定靶点的途径,以改善对这种破坏性的、目前难以治疗的疾病的治疗。

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Keloids: Animal models and pathologic equivalents to study tissue fibrosis.瘢痕疙瘩:用于研究组织纤维化的动物模型及病理对应物。
Matrix Biol. 2016 Apr;51:47-54. doi: 10.1016/j.matbio.2016.01.014. Epub 2016 Jan 29.
2
Skin tissue repair: Matrix microenvironmental influences.皮肤组织修复:基质微环境的影响
Matrix Biol. 2016 Jan;49:25-36. doi: 10.1016/j.matbio.2015.08.001. Epub 2015 Aug 14.
3
The extracellular matrix and transforming growth factor-β1: Tale of a strained relationship.细胞外基质与转化生长因子-β1:一段紧张关系的故事。
瘢痕疙瘩超级增强子网络的综合分析揭示了FOXP1介导的纤维化抗衰老机制。
Cell Mol Biol Lett. 2025 Jul 23;30(1):88. doi: 10.1186/s11658-025-00763-1.
4
Therapeutic potential of ginsenosides in circadian rhythm-based skin disorders.人参皂苷在基于昼夜节律的皮肤疾病中的治疗潜力。
J Ginseng Res. 2025 Jul;49(4):366-375. doi: 10.1016/j.jgr.2025.04.004. Epub 2025 Apr 15.
5
Keloids and hypertrophic scars in individuals with darker Fitzpatrick skin types: a systematic review of treatment efficacy and quality of life outcomes.Fitzpatrick皮肤类型较深的个体中的瘢痕疙瘩和增生性瘢痕:治疗效果和生活质量结局的系统评价
Arch Dermatol Res. 2025 Jun 3;317(1):795. doi: 10.1007/s00403-025-04292-x.
6
Unlocking Better Keloid Treatment: Corticosteroid, 5-Fluorouracil, and Hyaluronidase vs. Corticosteroid Alone - A Randomized Comparative Study.解锁更好的瘢痕疙瘩治疗方法:皮质类固醇、5-氟尿嘧啶和透明质酸酶与单独使用皮质类固醇的对比——一项随机对照研究。
Health Sci Rep. 2025 May 26;8(5):e70883. doi: 10.1002/hsr2.70883. eCollection 2025 May.
7
Mendelian randomization analysis of the causal relationship between immune cells and keloid.免疫细胞与瘢痕疙瘩因果关系的孟德尔随机化分析
Dermatol Reports. 2025 May 23;17(2). doi: 10.4081/dr.2024.10106. Epub 2024 Oct 23.
8
FTO-mediated m6A demethylation of KLF4 promotes the proliferation and collagen deposition of keloid fibroblasts.FTO介导的KLF4的m6A去甲基化促进瘢痕疙瘩成纤维细胞的增殖和胶原沉积。
Toxicol Res (Camb). 2025 Apr 26;14(2):tfaf058. doi: 10.1093/toxres/tfaf058. eCollection 2025 Apr.
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Progress of ADAM17 in Fibrosis-Related Diseases.ADAM17在纤维化相关疾病中的研究进展。
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4
Keloid-derived keratinocytes acquire a fibroblast-like appearance and an enhanced invasive capacity in a hypoxic microenvironment in vitro.瘢痕疙瘩来源的角质形成细胞在体外低氧微环境中呈现成纤维细胞样外观并具有增强的侵袭能力。
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Matrix remodeling by MMPs during wound repair.基质金属蛋白酶在创伤修复过程中的基质重塑。
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Premature collagen fibril formation, fibroblast-mast cell interactions and mast cell-mediated phagocytosis of collagen in keloids.瘢痕疙瘩中胶原原纤维的过早形成、成纤维细胞与肥大细胞的相互作用以及肥大细胞介导的胶原吞噬作用。
Ultrastruct Pathol. 2015 Apr;39(2):95-103. doi: 10.3109/01913123.2014.981326. Epub 2015 Jan 8.
8
The α4β1 integrin and the EDA domain of fibronectin regulate a profibrotic phenotype in dermal fibroblasts.α4β1整合素与纤连蛋白的EDA结构域调节真皮成纤维细胞中的促纤维化表型。
Matrix Biol. 2015 Jan;41:26-35. doi: 10.1016/j.matbio.2014.11.004. Epub 2014 Nov 26.
9
Recent developments in the use of intralesional injections keloid treatment.瘢痕疙瘩治疗中病灶内注射使用的最新进展。
Arch Plast Surg. 2014 Nov;41(6):620-9. doi: 10.5999/aps.2014.41.6.620. Epub 2014 Nov 3.
10
Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans.混合映射确定了一个位于15q21.2 - 22.3的基因座,该基因座与非裔美国人的瘢痕疙瘩形成有关。
Hum Genet. 2014 Dec;133(12):1513-23. doi: 10.1007/s00439-014-1490-9. Epub 2014 Oct 4.