Jia Guanghong, Sowers James R
Divisions of Endocrinology, Diabetes, Hypertension and Metabolism, Diabetes Cardiovascular Center, University of Missouri School of Medicine, Columbia, MO, USA; Harry S. Truman Memorial Veterans Hospital, University of Missouri School of Medicine, Columbia, MO, USA.
Divisions of Endocrinology, Diabetes, Hypertension and Metabolism, Diabetes Cardiovascular Center, University of Missouri School of Medicine, Columbia, MO, USA; Departments of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, USA; Harry S. Truman Memorial Veterans Hospital, University of Missouri School of Medicine, Columbia, MO, USA.
Biochim Biophys Acta. 2015 Feb;1852(2):219-24. doi: 10.1016/j.bbadis.2014.06.025. Epub 2014 Jun 28.
Autophagy, literally translated means self-eating, is a primary degradative pathway and plays an important role in the regulation of cellular homeostasis through elimination of aggregated proteins, damaged organelles, and intracellular pathogens. Autophagy has been classified into microautophagy, macroautophagy, and chaperone-mediated autophagy, depending on the choice of the pathway by which the cellular material is delivered to lysosomes. Dysregulation of autophagy may contribute to the development of cardiorenal metabolic syndrome (CRS), including insulin resistance, obesity, hypertension, maladaptive immune modulation, and associated cardiac and renal disease. Clarifying the pathways and mechanisms of autophagy under normal conditions is essential to understanding its dysregulation in the development of CRS. Here, we highlight a recent surge in autophagy research, such as the cellular quality control through the disposal and recycling of cellular components, and summarize our contemporary understanding of molecular mechanisms of autophagy in diverse organ or tissues involved in the pathogenesis of CRS. This article is part of a Special Issue entitled: Autophagy and protein quality control in cardiometabolic diseases.
自噬，字面意思是“自我吞噬”，是一种主要的降解途径，通过清除聚集的蛋白质、受损的细胞器和细胞内病原体，在调节细胞内稳态中发挥重要作用。根据细胞物质被输送到溶酶体的途径选择，自噬可分为微自噬、巨自噬和伴侣介导的自噬。自噬失调可能导致心肾代谢综合征（CRS）的发生，包括胰岛素抵抗、肥胖、高血压、适应性免疫调节异常以及相关的心脏和肾脏疾病。阐明正常条件下自噬的途径和机制对于理解其在CRS发生发展中的失调至关重要。在此，我们重点介绍了自噬研究的最新进展，如通过细胞成分的处理和再循环进行细胞质量控制，并总结了我们目前对参与CRS发病机制的不同器官或组织中自噬分子机制的理解。本文是名为“心血管代谢疾病中的自噬与蛋白质质量控制”特刊的一部分。
