Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, United States.
Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, United States.
Front Cell Infect Microbiol. 2021 Jun 9;11:693051. doi: 10.3389/fcimb.2021.693051. eCollection 2021.
is a digenetic parasite that requires triatomines and mammalian host to complete its life cycle. replication in mammalian host induces immune-mediated cytotoxic proinflammatory reactions and cellular injuries, which are the common source of reactive oxygen species (ROS) and reactive nitrogen species (RNS) during the acute parasitemic phase. Mitochondrial dysfunction of electron transport chain has been proposed as a major source of superoxide release in the chronic phase of infection, which renders myocardium exposed to sustained oxidative stress and contributes to Chagas disease pathology. Sirtuin 1 (SIRT1) is a class III histone deacetylase that acts as a sensor of redox changes and shapes the mitochondrial metabolism and inflammatory response in the host. In this review, we discuss the molecular mechanisms by which SIRT1 can potentially improve mitochondrial function and control oxidative and inflammatory stress in Chagas disease.
克氏锥虫是一种双生性寄生虫,需要通过三锥虫和哺乳动物宿主才能完成其生命周期。在哺乳动物宿主体内的复制会引起免疫介导的细胞毒性促炎反应和细胞损伤,这是急性寄生虫血症阶段产生活性氧(ROS)和活性氮(RNS)的常见来源。电子传递链的线粒体功能障碍被认为是感染慢性阶段超氧化物释放的主要来源,这使得心肌暴露于持续的氧化应激下,并导致恰加斯病的病理。沉默信息调节因子 1(SIRT1)是一种 III 类组蛋白去乙酰化酶,可作为氧化还原变化的传感器,并调节宿主的线粒体代谢和炎症反应。在这篇综述中,我们讨论了 SIRT1 可能改善恰加斯病中线粒体功能和控制氧化和炎症应激的分子机制。