Hirota Kiichi
Department of Anesthesiology, Kansai Medical University, 2-3-1 Shin-Machi, Hirakata, Osaka 573-1191, Japan.
Cardiovasc Hematol Disord Drug Targets. 2015;15(1):29-40. doi: 10.2174/1871529x15666150108115553.
Sepsis is a state of infection with serious systemic manifestations, and if severe enough, can be associated with multiple organ dysfunction and systemic hypotension, which can cause tissues to be hypoxic. Inflammation, as part of the multifaceted biological response to injurious stimuli, such as pathogens or damaged tissues and cells, underlies these biological processes. Prolonged and persistent inflammation, also known as chronic inflammation, results in progressive alteration in the various types of cells at the site of inflammation and is characterized by the simultaneous destruction and healing of tissue during the process. Tissue hypoxia during inflammation is not just a simple bystander process, but can considerably affect the development or attenuation of inflammation by causing the regulation of hypoxia-dependent gene expression. Indeed, the study of transcriptionally regulated tissue adaptation to hypoxia requires intense investigation to help control hypoxia-induced inflammation and organ failure. In this review, I have described the pathophysiology of sepsis with respect to oxygen metabolism and expression of hypoxia-inducible factor 1.
脓毒症是一种伴有严重全身表现的感染状态，若病情足够严重，可伴有多器官功能障碍和全身性低血压，进而导致组织缺氧。炎症作为对诸如病原体、受损组织和细胞等有害刺激的多方面生物学反应的一部分，是这些生物学过程的基础。持续时间较长的持续性炎症，即慢性炎症，会导致炎症部位各类细胞发生渐进性改变，其特征是在此过程中组织同时出现破坏和修复。炎症期间的组织缺氧并非简单的旁观者过程，而是可通过调控缺氧相关基因表达，对炎症的发展或减轻产生显著影响。事实上，对转录调控的组织缺氧适应的研究需要深入探究，以助力控制缺氧诱导的炎症和器官衰竭。在这篇综述中，我阐述了脓毒症在氧代谢及缺氧诱导因子1表达方面的病理生理学。
