高速泳动族蛋白B1和自噬在急性肺损伤致病中的作用机制

Study on the role of high mobility group box-1 and autophagy in acute lung injury

急性肺损伤(acute lung injury,ALI)是危重患者病程中出现的一种危及生命的临床综合征。鉴定早期诊断ALI的新型生物标志物和寻找更有效的治疗方法是当前研究的热点。高速泳动族蛋白B1(high mobility group box-1 protein,HMGB1)是一种与脓毒症、恶性肿瘤和免疫性疾病密切相关的晚期炎症介质。HMGB1水平表达可反映机体炎症和组织损伤的严重程度,提示其在ALI患者预后生物标志物的潜在作用,以及作为阻断机体炎症通路的潜在靶点。多项研究表明,HMGB1可调节自噬。自噬或称Ⅱ型程序性细胞死亡,是维持细胞内环境稳定的重要生物学过程。研究显示,HMGB1和自噬参与包括ALI在内的多种肺部疾病的致病过程,具体机制仍需进一步明确。本文系统阐述HMGB1和自噬在ALI致病中的作用。

Acute lung injury(ALI)is a life-threatening clinical syndrome during the clinical course in critically ill patients. The identification of novel biomarkers for early diagnosis and finding more effective treatments of ALI are topics on current research. High mobility group box-1 protein(HMGB1) is a late inflammatory mediator associated with sepsis,malignancy,and immune disease.Expression of HMGB1 may reflect the severity of inflammation and tissue damage,which indicates a potential role for HMGB1 as a prognostic biomarker and a potential target for blocking inflammatory pathways in ALI. Several studies have shown that HMGB1 regulates autophagy. Autophagy,also called type Ⅱ programmed cell death,is an important biological process which maintains cellular homeostasis. Studies have shown that HMGB1 and autophagy are involved in the pathogenesis of many lung diseases including ALI,while the underlying specific mechanisms remain to be determined. This review provides an update on the role of HMGB1 and autophagy in ALI.