Autophagy Role in Cardiovascular Diseases

About this Research Topic

Background

Macroautophagy (autophagy) is a lysosome-dependent degradation process that is essential for intracellular protein catabolism and organelle quality control. Autophagy attenuation was found in aging, atherosclerosis, diabetes and neurodegenerative diseases. However, the role of autophagy in cardiology and heart pathology has not been evaluated sufficiently until now.

Coronary heart diseases are the leading cause of cardiovascular death. Cardiac aging is characterized by the presence of hypertrophy, fibrosis, and accumulation of misfolded proteins and dysfunctional mitochondria. Autophagy and autophagic flux are generally decreased in aging hearts, and murine autophagy loss-of-function models develop exacerbated cardiac dysfunction that is accompanied by the accumulation of misfolded proteins and dysfunctional organelles. In coronary heart diseases autophagy and apoptosis are two forms of programmed cell deaths which are important in the pathogenesis, development and prognosis of these diseases. Activated autophagy can protect heart from myocardial ischemia injury and post-ischemia cardiac remodeling, however also can exert controversial effects on ischemia/reperfusion injury and coronary atherosclerosis. Some drugs and pharmacologic compounds (mTOR inhibitor and AMPK activator) have been reported to regulate autophagy and apoptosis. Recent studies are limited and insufficient, they have pointed out the complex interplay between autophagy and apoptosis and further provided treatment concept for coronary heart disease by balancing the switch between the two responses.

It has been shown that dysregulation of autophagy in cardiomyocytes is involved in cardiac hypertrophy, myocardial infarction, diabetic cardiomyopathy, and heart failure. So, autophagy seems to be an attractive therapeutic target for cardiac diseases.

Stimulation of autophagy generally improves cardiac function in mouse models of protein aggregation by removing accumulated misfolded proteins, dysfunctional mitochondria, and damaged DNA, thereby improving the overall cellular environment and alleviating aging-associated pathology in the heart. These evidences suggest that autophagy is required for many mechanisms that mediate lifespan extension, such as caloric restriction, in various organisms. Autophagy may play an important role in combating the adverse effects of aging in the heart diseases. Possibly, regulated forms of cardiomyocyte death play important roles in both myocardial infarction with reperfusion (ischemia/reperfusion) and heart failure.

The molecular mechanisms that stimulate autophagy include the activation of energy deprivation sensors, (sirtuin-1 (SIRT1) and adenosine monophosphate-activated protein kinase, AMPK). These enzymes also enhance autophagic flux, which leads to the removal of dysfunctional mitochondria and peroxisomes. Type 2 diabetes is characterized by suppression of SIRT1 and AMPK signaling as well as an impairment of autophagy. A model of type 2 diabetes in db/db mice is characterized by a deletion of the leptin receptor gene, which leads to obesity, insulin resistance, metabolic syndrome development and type 2 diabetes.

Autophagy is generally induced by stress, such as oxygen-, energy- or amino acid-deprivation, irradiation, effect of some drugs. In addition to non-selective bulk degradation, autophagy also occurs in a selective manner, recycling specific organelles, such as mitochondria, peroxisomes, ribosomes, endoplasmic reticulum, lysosomes, nuclei, proteasomes and lipid droplets. This capability makes selective autophagy a major process in maintaining cellular homeostasis.

It is important to focus on the role of autophagy in various cardiac diseases and the pharmacological basis and therapeutic potential of medical drugs and natural products in cardiac diseases by modifying autophagic processes.

Keywords: autophagy, selective autophagy and mitophagy, autophagy inductors, trehalose, metformin, dislipidemia, atherosclerosis, diabetes

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