脓毒症病理生理及信号转导机制的研究进展
Progress of study on pathophysiology and signal transduction pathways of sepsis
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摘要: 脓毒症作为重症监护室常见的危重症之一,过去几十年来,其发病率及病死率并未得到有效改善。最新的脓毒症定义中指出要及时认识到宿主针对感染所出现的反应失调,因为由此导致的器官功能障碍将会极大影响患者生存率。本文从脓毒症定义及流行病学数据出发,按照炎症反应,凝血功能障碍,免疫应答抑制,器官功能障碍等角度探讨了脓毒症的病理生理机制,同时介绍了核因子κB(NF-κB), Janus激酶/信号转导与转录激活子(JAK/STAT),磷酸肌苷3-激酶/丝氨酸/苏氨酸激酶(PI3K/Akt),丝裂原活化蛋白激酶(MAPK)等信号通路,从信号转导机制水平就近年来脓毒症的研究进展做以总结。以期为脓毒症临床研究及防治工作奠定理论基础,最终提高脓毒症的救治水平。Abstract: Sepsis is one of the common critical diseases in intensive care unit (ICU), and the morbidity and mortality of sepsis remained high over the past decades. The latest definition of sepsis calls for timely recognition of the dysregulated host response to infection, as the resulting organ dysfunction can greatly endanger a patient’s life. Based on the definition and epidemiological data of sepsis, the pathophysiology of sepsis was discussed from the perspectives of inflammation, coagulation dysfunction, immunosuppression and organ dysfunction. At the same time, the nuclear factor κB(NF-κB), Janus kinase (JAK)/signal transduction and activator of transcription (STAT), phosphate inosine 3-kinase (PI3K)/ serine/threonine kinase (Akt) and mitogen-activated protein kinase (MAPK) were introduced to summarize the progress of research on sepsis. It is expected to lay a theoretical foundation for clinical research and prevention of sepsis and ultimately improve the treatment level of sepsis.
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