HMGB1在脓毒性急性肺损伤中的调控机制
The Regulatory Mechanism of HMGB1 in Septic Acute Lung Injury
摘要: 急性肺损伤(Acute Lung Injury, ALI)是脓毒症常见的临床并发症之一,其发病机制包含复杂的炎症反应与细胞损伤,高迁移率族蛋白B1 (High mobility group box 1, HMGB1)属于脓毒症急性肺损伤后期产生的炎症介质,在该病病理进程中起到重要的调节效果。这篇文献综述汇总了脓毒症急性肺损伤的发病机理,并着重论述了HMGB1的调节功效及同其它炎症介质之间的交互情况。研究成果显示,HMGB1可以在细胞质中调控肺泡巨噬细胞的自噬与凋亡从而起到保护作用,同时在炎症等应激条件下,HMGB1转移至细胞外引起炎症因子的过度激活,导致肺损伤。二者结合影响着脓毒症急性肺损伤的严重程度和预后情况,这或许意味着HMGB1成为了脓毒症急性肺损伤潜在的医治靶标,给临床上的干预策略给予了新方向。
Abstract: Acute Lung Injury (ALI) is one of the common clinical complications of sepsis, the pathogenesis of which involves complex inflammatory response and cellular damage, and High mobility group box 1 (HMGB1) belongs to the inflammatory mediators produced in the late stage of acute lung injury in sepsis, and plays an important regulatory role in the pathological process of this disease. This review summarizes the pathogenesis of acute lung injury in sepsis and focuses on the regulatory effects of HMGB1 and its interactions with other inflammatory mediators. The results show that HMGB1 regulates autophagy and apoptosis in alveolar macrophages in the cytoplasm to play a protective role, while under stress conditions such as inflammation, HMGB1 translocates to the extracellular compartment to cause hyperactivation of inflammatory factors, leading to lung injury. The combination of the two influences the severity and prognosis of acute lung injury in sepsis, which may imply that HMGB1 has become a potential therapeutic target for acute lung injury in sepsis, giving a new direction for clinical intervention strategies.
文章引用:李铠君, 黎雨茜, 孙雪东. HMGB1在脓毒性急性肺损伤中的调控机制[J]. 临床医学进展, 2025, 15(7): 387-392. https://doi.org/10.12677/acm.2025.1572000

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