Wang Zheng-Cai, Zhao Wan-Yi, Cao Yangyang, Liu Yan-Qi, Sun Qihang, Shi Peng, Cai Jia-Qin, Shen Xiao Z, Tan Wei-Qiang
Department of Plastic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.
Front Immunol. 2020 Dec 4;11:603187. doi: 10.3389/fimmu.2020.603187. eCollection 2020.
The underlying mechanisms of wound healing are complex but inflammation is one of the determining factors. Besides its traditional role in combating against infection upon injury, the characteristics and magnitude of inflammation have dramatic impacts on the pathogenesis of scar. Keloids and hypertrophic scars are pathological scars that result from aberrant wound healing. They are characterized by continuous local inflammation and excessive collagen deposition. In this review, we aim at discussing how dysregulated inflammation contributes to the pathogenesis of scar formation. Immune cells, soluble inflammatory mediators, and the related intracellular signal transduction pathways are our three subtopics encompassing the events occurring in inflammation associated with scar formation. In the end, we enumerate the current and potential medicines and therapeutics for suppressing inflammation and limiting progression to scar. Understanding the initiation, progression, and resolution of inflammation will provide insights into the mechanisms of scar formation and is useful for developing effective treatments.
伤口愈合的潜在机制很复杂，但炎症是决定性因素之一。除了其在损伤后对抗感染的传统作用外，炎症的特征和程度对瘢痕的发病机制有显著影响。瘢痕疙瘩和增生性瘢痕是异常伤口愈合导致的病理性瘢痕。它们的特征是局部炎症持续和胶原蛋白过度沉积。在本综述中，我们旨在讨论炎症失调如何导致瘢痕形成的发病机制。免疫细胞、可溶性炎症介质和相关的细胞内信号转导途径是我们涵盖与瘢痕形成相关炎症中发生事件的三个子主题。最后，我们列举了目前和潜在的用于抑制炎症和限制瘢痕进展的药物和治疗方法。了解炎症的起始、进展和消退将为瘢痕形成机制提供见解，并有助于开发有效的治疗方法。
