de Andrade Ramos Bruna Ribeiro, Witkin Steven S
Department of Pathology, Botucatu Medical School, São Paulo State University-UNESP, Distrito de Rubião Júnior, 18618-970, Botucatu, São Paulo, Brazil.
Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, NY, USA.
Cell Stress Chaperones. 2016 Sep;21(5):755-62. doi: 10.1007/s12192-016-0715-3. Epub 2016 Jul 6.
The generation of reactive oxygen species (ROS), a byproduct of aerobic energy metabolism, is maintained at physiological levels by the activity of antioxidant components. Insufficiently opposed ROS results in oxidative stress characterized by altered mitochondrial function, decreased protein activity, damage to nucleic acids, and induction of apoptosis. Elevated levels of inadequately opposed ROS induce autophagy, a major intracellular pathway that sequesters and removes damaged macromolecules and organelles. In early pregnancy, autophagy induction preserves trophoblast function in the low oxygen and nutrient placental environment. Inadequate regulation of the ROS-autophagy axis leads to abnormal autophagy activity and contributes to the development of preeclampsia and intrauterine growth restriction. ROS-autophagy interactions are altered at the end of gestation and participate in the initiation of parturition at term. The induction of high levels of ROS coupled with a failure to induce a corresponding increase in autophagy results in the triggering of preterm labor and delivery.
活性氧（ROS）是有氧能量代谢的副产物，通过抗氧化成分的活性将其维持在生理水平。ROS未得到充分对抗会导致氧化应激，其特征为线粒体功能改变、蛋白质活性降低、核酸损伤以及细胞凋亡诱导。未得到充分对抗的ROS水平升高会诱导自噬，这是一种主要的细胞内途径，可隔离并清除受损的大分子和细胞器。在妊娠早期，自噬诱导可在低氧和营养缺乏的胎盘环境中维持滋养层功能。ROS-自噬轴调节不足会导致自噬活性异常，并促进子痫前期和胎儿生长受限的发展。ROS-自噬相互作用在妊娠末期发生改变，并参与足月分娩的启动。高水平ROS的诱导加上未能诱导自噬相应增加会导致早产和分娩。
