Acne is a common chronic inflammatory dermatosis that can lead to pathological scars (PSs, divided into hypertrophic scars and keloids). These kinds of abnormal scars seriously reduce the quality of life of patients. However, their mechanism is still unclear, resulting in difficult clinical prevention, unstable treatment effects and a high risk of recurrence. Available evidence supports inflammatory changes caused by infection as one of the keys to abnormal proliferation of skin fibroblasts. In acne-induced PSs, increasing knowledge of the immunopathology indicates that inflammatory cells directly secrete growth factors to activate fibroblasts and release pro-inflammatory factors to promote the formation of PSs. T helper cells contribute to PSs via the secretion of interleukin (IL)-4 and IL-13, the pro-inflammatory factors; while regulatory T cells have anti-inflammatory effects, secrete IL-10 and prostaglandin E2, and suppress fibrosis production. Several treatments are available, but there is a lack of combination regimens to target different aspects of acne-induced PSs. Overall, this review indicates that the joint involvement of inflammatory response and fibrosis plays a crucial role in acne-induced PSs, and also analyzes the interaction of current treatments for acne and PS.

中文翻译：

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痤疮引起的病理性疤痕：病理生理学和当前治疗方法


痤疮是一种常见的慢性炎症性皮肤病，可导致病理性疤痕（PS，分为肥厚性疤痕和疤痕疙瘩）。这类异常疤痕严重降低了患者的生活质量。但其作用机制尚不明确，导致临床预防困难、治疗效果不稳定、复发风险高。现有证据支持感染引起的炎症变化是皮肤成纤维细胞异常增殖的关键之一。在痤疮诱导的 PS 中，越来越多的免疫病理学知识表明炎症细胞直接分泌生长因子来激活成纤维细胞并释放促炎因子以促进 PS 的形成。 T 辅助细胞通过分泌白细胞介素 (IL)-4 和 IL-13（促炎因子）促进 PS；而调节性T细胞则具有抗炎作用，分泌IL-10和前列腺素E2，并抑制纤维化的产生。有多种治疗方法可供选择，但缺乏针对痤疮引起的 PS 不同方面的联合治疗方案。总的来说，这篇综述表明炎症反应和纤维化的共同参与在痤疮诱发的 PS 中起着至关重要的作用，并且还分析了当前痤疮和 PS 治疗的相互作用。