Department of Anesthesiology and Critical Care, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA.
Crit Care Clin. 2010 Jul;26(3):567-75, x-xi. doi: 10.1016/j.ccc.2010.04.007.
Sepsis is among the most common causes of death in patients in intensive care units in North America and Europe. In the United States, it accounts for upwards of 250,000 deaths each year. Investigations into the pathobiology of sepsis have most recently focused on common cellular and subcellular processes. One possibility would be a defect in the production of energy, which translates to an abnormality in the production of adenosine triphosphate and therefore in the function of mitochondria. This article presents a clear role for mitochondrial dysfunction in the pathogenesis and pathophysiology of sepsis. What is less clear is the teleology underlying this response. Prolonged mitochondrial dysfunction and impaired biogenesis clearly are detrimental. However, early inhibition of mitochondrial function may be adaptive.
脓毒症是北美和欧洲重症监护病房患者死亡的最常见原因之一。在美国，每年有超过 25 万人因此死亡。最近对脓毒症病理生物学的研究主要集中在常见的细胞和亚细胞过程上。一种可能性是能量产生缺陷，这意味着三磷酸腺苷的产生异常，因此线粒体的功能也异常。本文提出了线粒体功能障碍在脓毒症发病机制和病理生理学中的明确作用。不太清楚的是这种反应的目的论。线粒体功能障碍持续时间长且生物发生受损显然是有害的。然而，早期抑制线粒体功能可能是适应性的。
