瘢痕疙瘩发病机制的研究进展  

Research progress in the pathogenesis of keloids

作　　者：贾坤朋 周婧[1] JIA Kunpeng;ZHOU Jing(Second Affiliated Hospital of Harbin Medical University,Harbin 150000,China)

机构地区：[1]哈尔滨医科大学附属第二医院皮肤科,黑龙江哈尔滨150000

出　　处：《皮肤性病诊疗学杂志》2023年第2期176-180,共5页Journal of Diagnosis and Therapy on Dermato-venereology

摘　　要：皮肤创伤愈合过程中,成纤维细胞过度增殖、细胞外基质中胶原过度沉积,形成一种以侵袭性生长为特点的良性肿瘤—瘢痕疙瘩。瘢痕疙瘩是一个具有挑战性的医学问题,大多数传统治疗方法效果不佳,且复发率高。其发病机制十分复杂,尚有许多争议。本文对炎症反应、机械力、表观遗传修饰等瘢痕疙瘩形成机制研究进展进行综述,表明瘢痕疙瘩的形成是多种因素共同作用的结果,中性粒细胞、巨噬细胞、肥大细胞、T淋巴细胞等炎症细胞,白介素-6(IL-6)、TGF-β、TNF-α等炎症因子,整合素信号通路、TGF-β/Smad信号通路、Rho-GTP酶、YAP/TAZ、Wnt/β-catenin信号通路等机械力因素以及表观遗传修饰、脂联素均与瘢痕疙瘩的形成有关,对上述因素的干预有望成为治疗瘢痕疙瘩的新方法。During the process of skin wound healing,hyperproliferation of fibroblasts and excessive deposition of collagen in the extracellular matrix lead to the formation of keloid,a benign tumor with characteristics of aggressive growth.Keloid is a challenging medical problem.The therapeutic efficacies of most conventional approaches are unsatisfactory.Keloid has a higher recurrence rate with a complex pathogenesis.This article reviews the progress of research in the formation of keloid,including inflammation,mechanical forces,epigenetic modification and so on,Studies show that interaction of multiple factors is involved in the formation of keloid,including inflammatory cells(neutrophils,macrophages,mast cells and T lymphocytes),inflammatory cytokines(interleukin-6,TGF-βand TNF-α),integrin signaling pathway,TGF-β/Smad signaling pathway,Rho-GTPase,YAP/TAZ,Wnt/β-catenin signaling pathway,epigenetic modification and adiponectin.The intervention of these factors is expected to become a new approach for the treatment of keloid.

关 键 词：瘢痕疙瘩 发病机制 炎症 机械力 

分 类 号：R751[医药卫生—皮肤病学与性病学]