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伤口愈合过程中的炎症反应:系统性审查
Fernanda Barbosa Lopes1, Mariáurea Matias Sarandy1,2, Rômulo Dias Novaes3,4
1Department of General Biology, Federal University of Viçosa, Viçosa 36570-900, Minas Gerais, Brazil.
Antioxidants (Basel, Switzerland)
|July 27, 2024
概括
这项研究揭示了氧化应激和炎症在皮肤伤口愈合中如何相互作用. 准NLRP3炎症酶和相关途径可能会导致更好的慢性伤口治疗.
科学领域:
- 免疫学 免疫学 免疫学
- 皮肤病学 皮肤病学
- 分子生物学分子生物学
背景情况:
- 皮肤伤口愈合涉及复杂的炎症和修复过程.
- 目前的治疗方法旨在控制炎症并加速皮肤的修复,但仍然存在挑战.
- 了解皮肤伤口愈合的分子机制对于开发有效疗法至关重要.
研究的目的:
- 调查皮肤伤口愈合背后的关键机制.
- 为开发针对氧化性炎症和感染的新疗法提供见解.
- 为了减少伤口管理中的功能损失和相关成本.
主要方法:
- 在遵守PRISMA指南的基础上进行系统审查.
- 在MEDLINE (PubMed),Scopus和Web of Science数据库中进行的搜索.
- 使用SYRCLE工具分析了23项具有偏见和质量评估的原始研究.
主要成果:
- 早期的伤口愈合涉及到细胞 (特别是巨细胞) 上的膜受体 (IFN-δ,TNF-α,toll-like) 的激活.
- STAT1,IP3和NF-kβ通路的上调;Ca2+调动与ROS产生和NLRP3炎症酶激活相关.
- 这导致caspase-1裂变,释放IL-1β和IL-18,随后释放IL-1,iNOS,TNF-α和TGF-β等介质,创造一种亲氧化环境并削弱抗氧化防御.
结论:
- 在IFN-δ,ROS生产和炎症标志物之间存在积极的反循环,加剧氧化应激和炎症.
- NLRP3炎症酶激活,ROS和促炎细胞因子有助于慢性炎症和组织损伤.
- 针对这些相互连接的途径提供了改善伤口愈合治疗策略的潜力.
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