Special Issue "Role of Mitochondria and Autophagy in the Pathogenesis of Atherosclerosis"
Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 4550
2. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Valencia, Spain
3. Departamento de Fisiología, Facultad de Medicina, Universidad de Valencia, Valencia, Spain
Interests: mitochondria; autophagy; type 2 diabetes; oxidative stress; mitophagy; insulin resistance; atherosclerosis
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It is well known that oxidative stress, mitochondrial dysfunction, and autophagy are related to the pathogenesis of atherosclerosis and cardiovascular diseases (CVD). Atherosclerosis represents a state of exacerbated oxidative stress characterized by protein and lipid oxidation in the vascular endothelium. High production of reactive oxygen species (ROS) in mitochondria, mitochondrial DNA damage, and respiratory chain impairment have all been related to atherosclerosis or cardiomyopathy in human and animal studies. Furthermore, they are major precursors of atherosclerosis-hypercholesterolemia, hyperglycemia, hypertriglyceridemia, and aging-induced mitochondrial dysfunction. Chronic overproduction of mitochondrial ROS can lead to increased oxidation of low-density lipoproteins, pancreatic beta-cell impairment, and dysfunction of endothelial cell-factors that promote atherosclerosis. Mitochondrial function is required for normal vascular cell growth and function, and mitochondrial dysfunction can result in apoptosis, favoring the atherosclerotic process and plaque rupture.
Autophagy is the process of nonselective degradation of proteins, lipids, and organelles, and occurs in response to internal or external stimuli, such as oxidative stress, the unfolded protein response (UPR), the malfunctioning of organelles (internal inductors) and growth factors, serum starvation and amino acid deprivation (external stimuli). In this sense, autophagy is a survival mechanism and a strictly regulated process. Different studies point to the critical and defensive role of autophagy in vascular cells against different insults.
It is clear that oxidative stress, mitochondrial function, and autophagy are key factors in the modulation and progression of atherosclerosis. Major ROS-sensitive signal transduction pathways, mitochondrial alterations, and changes in the autophagic process are now known to be involved in atherosclerosis, but there is still much to be learned about their mutual interaction and the modifications they undergo during metabolic and vascular diseases, including type 2 diabetes. Given the relevance of this topic, it would seem appropriate to summarize some of the main recent advances in research on the role of vascular oxidative stress, mitochondrial function and autophagy in the pathogenesis of atherosclerosis and their impact on health, disease, and aging.
We invite authors to submit original articles and review articles on this interesting topic.
Prof. Dr. Victor M. Victor
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- Oxidative stress
- Type 2 diabetes