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Role of Mitochondria and Autophagy in the Pathogenesis of Atherosclerosis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Vascular Medicine".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 5765

Special Issue Editor


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Guest Editor
1. FISABIO–Hospital Universitario Dr. Peset, Valencia, Spain
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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Special Issue Information

Dear Colleagues,

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
Guest Editor

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Keywords

  • Atherosclerosis
  • Autophagy
  • Endothelium
  • Inflammation
  • Mitochondria
  • Mitophagy
  • Oxidative stress
  • Type 2 diabetes
  • Vascular

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Published Papers (2 papers)

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Research

19 pages, 6572 KiB  
Article
Association between Proinflammatory Markers, Leukocyte–Endothelium Interactions, and Carotid Intima–Media Thickness in Type 2 Diabetes: Role of Glycemic Control
by Aranzazu Martinez de Marañón, Francesca Iannantuoni, Zaida Abad-Jiménez, Francisco Canet, Pedro Díaz-Pozo, Sandra López-Domènech, Ildefonso Roldán-Torres, Carlos Morillas, Milagros Rocha and Víctor M. Víctor
J. Clin. Med. 2020, 9(8), 2522; https://doi.org/10.3390/jcm9082522 - 5 Aug 2020
Cited by 8 | Viewed by 2891
Abstract
Glycated hemoglobin monitorization could be a tool for maintaining type 2 diabetes (T2D) under control and delaying the appearance of cardiovascular events. This cross-sectional study was designed to assess the role of glycemic control in modulating early-stage markers of cardiovascular complications. One hundred [...] Read more.
Glycated hemoglobin monitorization could be a tool for maintaining type 2 diabetes (T2D) under control and delaying the appearance of cardiovascular events. This cross-sectional study was designed to assess the role of glycemic control in modulating early-stage markers of cardiovascular complications. One hundred and eight healthy controls and 161 type 2 diabetic patients were recruited and distributed according to their glycemic control, setting the threshold at 6.5% (good control). Biochemical and anthropometrical parameters were registered during the initial visit, and peripheral blood was extracted to obtain polymorphonuclear cells and analyze inflammatory markers, adhesion molecules, leukocyte–endothelium interactions, and carotid intima–media thickness. Correlations between these parameters were explored. We found that inflammatory markers and adhesion molecules were augmented in type 2 diabetic subjects with poor glycemic control. Polymorphonuclear leukocytes interacted more with the endothelium in the diabetic population, and even more significantly in the poorly controlled subjects. In parallel, carotid intima–media thickness was also increased in the diabetic population, and the difference was greater among poorly controlled subjects. Finally, correlation measurement revealed that carotid intima–media thickness was related to glycemic control and lipid metabolism in diabetic patients. Our results suggest that glycemic control delays the onset of cardiovascular comorbidities in diabetic subjects. Full article
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14 pages, 2420 KiB  
Article
Mitochondrial Alterations and Enhanced Human Leukocyte/Endothelial Cell Interactions in Type 1 Diabetes
by Francesca Iannantuoni, Aranzazu M. de Marañon, Zaida Abad-Jiménez, Francisco Canet, Pedro Díaz-Pozo, Sandra López-Domènech, Carlos Morillas, Milagros Rocha and Víctor M. Víctor
J. Clin. Med. 2020, 9(7), 2155; https://doi.org/10.3390/jcm9072155 - 8 Jul 2020
Cited by 11 | Viewed by 2449
Abstract
Type 1 diabetes has been associated with oxidative stress. This study evaluates the rates of oxidative stress, mitochondrial function, leukocyte–endothelium interactions and adhesion molecules in type 1 diabetic patients. The study population consisted of 52 diabetic patients and 46 body-composition and age-matched controls. [...] Read more.
Type 1 diabetes has been associated with oxidative stress. This study evaluates the rates of oxidative stress, mitochondrial function, leukocyte–endothelium interactions and adhesion molecules in type 1 diabetic patients. The study population consisted of 52 diabetic patients and 46 body-composition and age-matched controls. We assessed anthropometric and metabolic parameters, oxidative stress and mitochondrial function by evaluating reactive oxygen species (ROS) production, mitochondrial ROS production, mitochondrial membrane potential and superoxide dismutase (SOD) and catalase (CAT) expression in polymorphonuclear leukocytes from type 1 diabetic patients. In addition, we evaluated interactions between leukocytes and human umbilical vein endothelial cells (HUVEC), and serum expression of adhesion molecules (P-selectin, VCAM-1 and ICAM-1), proinflammatory cytokines (IL-6 and TNFα) and myeloperoxidase (MPO). HbA1C and glucose levels were higher in diabetic patients than in control subjects, as expected. Mitochondrial function was altered and leukocyte–endothelium interactions were enhanced in diabetic patients, which was evident in the increase in total and mitochondrial ROS production, higher mitochondrial membrane potential, enhanced leukocyte rolling and adhesion, and decreased rolling velocity. Furthermore, we observed an increase in levels of adhesion molecules P-selectin, VCAM-1, and ICAM-1 in these subjects. In addition, type 1 diabetic patients exhibited an increase in proinflammatory mediators TNFα and MPO, and a decreased expression of SOD. The enhancement of leukocyte–endothelium interactions and proinflammatory markers correlated with glucose and HbA1Clevels. Mitochondrial alteration, oxidative stress, and enhanced leukocyte–endothelium interactions are features of type 1 diabetes and may be related to cardiovascular implications. Full article
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