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.
Keywords: Autophagy; Cardiorenal metabolic syndrome; Endoplasmic reticulum stress; Insulin resistance; Obesity; Reactive oxygen species.
Copyright © 2014. Published by Elsevier B.V.