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Integrins as a bridge between bacteria and cells: key targets for therapeutic wound healing
Burns & Trauma ( IF 6.3 ) Pub Date : 2024-07-16 , DOI: 10.1093/burnst/tkae022
Dong Yu 1, 2 , Zhaoyu Lu 1, 2 , Yang Chong 1, 2
Affiliation  

Integrins are heterodimers composed of α and β subunits that are bonded through non-covalent interactions. Integrins mediate the dynamic connection between extracellular adhesion molecules and the intracellular actin cytoskeleton. Integrins are present in various tissues and organs where these heterodimers participate in diverse physiological and pathological responses at the molecular level in living organisms. Wound healing is a crucial process in the recovery from traumatic diseases and comprises three overlapping phases: inflammation, proliferation and remodeling. Integrins are regulated during the entire wound healing process to enhance processes such as inflammation, angiogenesis and re-epithelialization. Prolonged inflammation may result in failure of wound healing, leading to conditions such as chronic wounds. Bacterial colonization of a wound is one of the primary causes of chronic wounds. Integrins facilitate the infectious effects of bacteria on the host organism, leading to chronic inflammation, bacterial colonization, and ultimately, the failure of wound healing. The present study investigated the role of integrins as bridges for bacteria–cell interactions during wound healing, evaluated the role of integrins as nodes for bacterial inhibition during chronic wound formation, and discussed the challenges and prospects of using integrins as therapeutic targets in wound healing.

中文翻译:


整合素作为细菌和细胞之间的桥梁:治疗性伤口愈合的关键靶点



整合素是由通过非共价相互作用结合的 α 和 β 亚基组成的异二聚体。整合素介导细胞外粘附分子和细胞内肌动蛋白细胞骨架之间的动态连接。整合素存在于各种组织和器官中,这些异二聚体在活生物体的分子水平上参与多种生理和病理反应。伤口愈合是创伤性疾病恢复的关键过程,包括三个重叠的阶段:炎症、增殖和重塑。整合素在整个伤口愈合过程中受到调节,以增强炎症、血管生成和上皮再形成等过程。长期炎症可能导致伤口愈合失败,导致慢性伤口等病症。伤口的细菌定植是慢性伤口的主要原因之一。整合素促进细菌对宿主生物体的感染作用,导致慢性炎症、细菌定植,并最终导致伤口愈合失败。本研究调查了整合素作为伤口愈合过程中细菌-细胞相互作用桥梁的作用,评估了整合素作为慢性伤口形成过程中细菌抑制节点的作用,并讨论了使用整合素作为伤口愈合治疗靶点的挑战和前景。
更新日期:2024-07-16
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