肥厚性瘢痕和瘢痕疙瘩的临床和分子研究:文献综述

Naina Banun Turobi, Fadel Rahman, Nathasya Fernanda, A. Fawzy
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摘要

背景:肥厚性疤痕和瘢痕疙瘩是伤口异常愈合的两种不同形式,其特点是纤维组织形成过多。尽管肥厚性疤痕和瘢痕疙瘩普遍存在,但人们对其发生和持续存在的病理生理机制仍不甚了解。这篇文献综述了目前对增生性疤痕和瘢痕疙瘩的临床和分子研究,旨在强调它们在病因、发病机制和治疗反应方面的差异。方法:对文献进行了全面审查,重点关注那些对增生性疤痕和瘢痕疙瘩的临床表现、遗传倾向、分子途径和治疗策略有重要见解的文章。其中包括实验研究和临床试验,以涵盖广泛的数据来源。结果:增生性疤痕局限于原来的伤口边界,随着时间的推移可能会消退,而瘢痕疙瘩则扩展到伤口边缘以外,不会消退。在临床上,增生性疤痕和瘢痕疙瘩在外观、质地和易发部位上都有所不同。在分子水平上,细胞因子表达、生长因子活性和细胞外基质组成的不同特征也凸显了这些差异。遗传学研究发现了几种易感因素,包括特定的基因突变和多态性。治疗策略各有不同,但皮质类固醇激素仍是治疗这两种疾病的一线疗法。针对特定分子通路的新兴疗法有望改善治疗效果。结论肥厚性疤痕和瘢痕疙瘩是一种复杂的疾病,具有不同的临床和分子特征。了解这些差异对于开发有针对性的有效疗法至关重要。未来的研究重点应放在揭示这些疾病的遗传基础和探索新的治疗靶点上。加强对致病机制的了解将有助于在增生性疤痕和瘢痕疙瘩的治疗中推进个性化医疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Clinical and Molecular Insights into Hypertrophic Scars and Keloids: A Literature Review
Background: Hypertrophic scars and keloids represent two distinct forms of abnormal wound healing, characterized by excessive fibrous tissue formation. Despite their prevalence, the pathophysiological mechanisms underlying their development and persistence remain incompletely understood. This literature review synthesizes current clinical and molecular insights into hypertrophic scars and keloids, aiming to highlight differences in their etiology, pathogenesis, and therapeutic responses. Methods: A comprehensive review of the literature was conducted, focusing on articles that provided significant insights into the clinical manifestations, genetic predispositions, molecular pathways, and treatment strategies related to hypertrophic scars and keloids. Experimental studies and clinical trials were included to encompass a wide range of data sources. Results: Hypertrophic scars are confined to the original wound boundary and may regress over time, whereas keloids extend beyond the wound margins and do not regress. Clinically, hypertrophic scars and keloids differ in their appearance, texture, and predilection sites. At the molecular level, these differences are underscored by distinct profiles of cytokine expression, growth factor activity, and extracellular matrix composition. Genetic studies have identified several predisposing factors, including specific gene mutations and polymorphisms. Treatment strategies vary; however, intralesional corticosteroids remain the first-line treatment for both conditions. Emerging therapies targeting specific molecular pathways offer potential for improved outcomes. Conclusion: Hypertrophic scars and keloids are complex conditions with distinct clinical and molecular characteristics. Understanding these differences is crucial for developing targeted and effective therapies. Future research should focus on unraveling the genetic basis of these conditions and exploring novel therapeutic targets. Enhanced knowledge of the pathogenic mechanisms will facilitate the advancement of personalized medicine approaches in the management of hypertrophic scars and keloids.
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