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首页> 外文期刊>Infectious Disorders - Drug Targets >Oxidative Stress and Mitochondrial Dysfunction in Sepsis: A Potential Therapy with Mitochondria-Targeted Antioxidants
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Oxidative Stress and Mitochondrial Dysfunction in Sepsis: A Potential Therapy with Mitochondria-Targeted Antioxidants

机译：败血症中的氧化应激和线粒体功能障碍：线粒体靶向抗氧化剂的潜在疗法。

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Sepsis and septic shock are the major causes of death in intensive care units. The prevalent hypothesis regarding the mechanisms of sepsis and septic shock indicates that this syndrome is caused by an excessive defensive and inflammatory response characterised by massive increases in reactive oxygen species (ROS), nitric oxide (NO) and inflammatory cytokines. The consequences of these syndromes are systemic damage to the vascular endothelium, impaired tissue and a compromised whole body respiration, glutathione depletion and mitochondrial respiratory dysfunction with diminished levels of ATP and O2 consumption. In general, ROS are essential to the functions of cells and particularly immune cells, but adequate levels of antioxidant defenses are required to protect against the harmful effects of excessive ROS production. Mitochondrial oxidative stress damage and dysfunction contribute to a number of cell pathologies that manifest themselves in a range of conditions, including sepsis. This review considers the process of sepsis from a mitochondrial perspective, discussing strategies for the targeted delivery of antioxidants to mitochondria currently under development. We will provide a summary of the following areas: the cellular metabolism of ROS and its role in pathophysiological processes such as sepsis; currently available antioxidants and possible reasons for their efficacy and inefficacy in ameliorating oxidative stress-mediated diseases; and recent developments in antioxidants that target the matrix-facing surface of the inner mitochondrial membrane in order to protect against mitochondrial oxidative damage, and their therapeutic potential as a treatment for sepsis.
机译：败血症和败血性休克是重症监护病房死亡的主要原因。关于败血症和败血性休克机制的普遍假设表明，该综合征是由过度的防御和炎症反应引起的，其特征在于活性氧（ROS），一氧化氮（NO）和炎症细胞因子的大量增加。这些综合症的后果是对血管内皮的全身性损伤，组织受损和全身呼吸受损，谷胱甘肽耗竭和线粒体呼吸功能障碍，同时ATP和O2消耗水平降低。通常，ROS对于细胞，特别是免疫细胞的功能至关重要，但是需要足够水平的抗氧化剂防御才能防止过度产生ROS的有害影响。线粒体氧化应激损伤和功能障碍导致许多细胞病变，这些疾病在包括败血症在内的一系列疾病中表现出来。这篇综述从线粒体的角度考虑了败血症的过程，讨论了将抗氧化剂靶向递送到线粒体中的策略。我们将提供以下方面的摘要：ROS的细胞代谢及其在诸如败血症等病理生理过程中的作用；当前可用的抗氧化剂及其在减轻氧化应激介导的疾病中功效和无效的可能原因；以及针对内线粒体膜面向基质表面的抗氧化剂的最新进展，以保护其免受线粒体氧化损伤，以及其作为败血症治疗的潜力。

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