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Cells
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Vascular Autophagy in Health and Disease
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Vascular Autophagy in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (1 June 2021) | Viewed by 19437

Special Issue Editors

Dr. Andreas Beyer

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Guest Editor
Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA
Interests: coronary artery disease; mitochondria; cardio-oncology; microcirculation
Special Issues, Collections and Topics in MDPI journals
Dr. William E. Hughes

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Assistant Guest Editor
Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA
Interests: autophagy; mitochondria; exercise physiology; microcirculation
Prof. Dr. J. David Symons

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Co-Guest Editor
Department of Nutrition and Integrative Physiology, College of Health; Division of Endocrinology, Metabolism, and Diabetes, School of Medicine; Investigator, Molecular Medicine Program, University of Utah, Salt Lake City, UT, USA
Interests: vascular physiology; endothelial cell metabolism; autophagy; sphingolipid metabolism

Special Issue Information

Dear Colleagues,

Autophagy is a basic cellular recycling process by which cells attempt to maintain homeostasis in response to various stressors (e.g., oxidative stress, hypoxia, and starvation) to continuously provide metabolic substrates during times of nutrient starvation. The process of autophagy has been well-described across many cell types in various species ranging from yeast to mammals, is relatively well-conserved evolutionarily, and contributes to the pathology of numerous chronic diseases. The underlying mechanisms and signaling pathways of autophagy have been extensively studied, but its role in the circulatory system remains relatively ill-defined. In this context, autophagy is an important process to maintain homeostasis within tissue that is exposed to a variety of physiological and pathophysiological stimuli.

This Special Issue will focus on the signaling mechanisms related to autophagy stimulation in heath and disease, as well as their functional relevance. Relevant topics include micro-autophagy, which directly envelops vesicles via direct invaginations within the membrane, and chaperone-mediated autophagy, which is specific to mammalian cells and involves the direct targeting and transportation of organelles that express specific molecular targets (e.g., mitophagy).

Dr. Andreas Beyer
Dr. William E. Hughes
Prof. Dr. J. David Symons
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • autophagy
  • mitophagy
  • coronary artery disease, type 2 diabetes mellitus, micro-vasculature, macro-vasculature

Published Papers (5 papers)

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Research

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19 pages, 3917 KiB  
Article
GDF-15 Deficiency Reduces Autophagic Activity in Human Macrophages In Vitro and Decreases p62-Accumulation in Atherosclerotic Lesions in Mice
by Aline Heduschke, Kathrin Ackermann, Beate Wilhelm, Lilli Mey, Gabriel Alejandro Bonaterra, Ralf Kinscherf and Anja Schwarz
Cells 2021, 10(9), 2346; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10092346 - 7 Sep 2021
Cited by 10 | Viewed by 2675
Abstract
(1) Background: Growth differentiation factor-15 (GDF-15) is associated with cardiovascular diseases and autophagy in human macrophages (MΦ). Thus, we are interested in investigating autophagic mechanisms with special respect to the role of GDF-15. (2) Methods: Recombinant (r)GDF-15 and siRNA GDF-15 were used to [...] Read more.
(1) Background: Growth differentiation factor-15 (GDF-15) is associated with cardiovascular diseases and autophagy in human macrophages (MΦ). Thus, we are interested in investigating autophagic mechanisms with special respect to the role of GDF-15. (2) Methods: Recombinant (r)GDF-15 and siRNA GDF-15 were used to investigate the effects of GDF-15 on autophagic and lysosomal activity, as well as autophagosome formation by transmission electron microscopy (TEM) in MΦ. To ascertain the effects of GDF-15−/− on the progression of atherosclerotic lesions, we used GDF-15−/−/ApoE−/− and ApoE−/− mice under a cholesterol-enriched diet (CED). Body weight, body mass index (BMI), blood lipid levels and lumen stenosis in the brachiocephalic trunk (BT) were analyzed. Identification of different cell types and localization of autophagy-relevant proteins in atherosclerotic plaques were performed by immunofluorescence. (3) Results: siGDF-15 reduced and, conversely, rGDF-15 increased the autophagic activity in MΦ, whereas lysosomal activity was unaffected. Autophagic degradation after starvation and rGDF-15 treatment was observed by TEM. GDF-15−/−/ApoE−/− mice, after CED, showed reduced lumen stenosis in the BT, while body weight, BMI and triglycerides were increased compared with ApoE−/− mice. GDF-15−/− decreased p62-accumulation in atherosclerotic lesions, especially in endothelial cells (ECs). (4) Conclusion: GDF-15 seems to be an important factor in the regulation of autophagy, especially in ECs of atherosclerotic lesions, indicating its crucial pathophysiological function during atherosclerosis development. Full article
(This article belongs to the Special Issue Vascular Autophagy in Health and Disease)
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17 pages, 3411 KiB  
Article
Hypertrophy-Reduced Autophagy Causes Cardiac Dysfunction by Directly Impacting Cardiomyocyte Contractility
by Christiane Ott, Tobias Jung, Sarah Brix, Cathleen John, Iris R. Betz, Anna Foryst-Ludwig, Stefanie Deubel, Wolfgang M. Kuebler, Tilman Grune, Ulrich Kintscher and Jana Grune
Cells 2021, 10(4), 805; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10040805 - 4 Apr 2021
Cited by 11 | Viewed by 2892
Abstract
Cardiac remodeling and contractile dysfunction are leading causes in hypertrophy-associated heart failure (HF), increasing with a population’s rising age. A hallmark of aged and diseased hearts is the accumulation of modified proteins caused by an impaired autophagy-lysosomal-pathway. Although, autophagy inducer rapamycin has been [...] Read more.
Cardiac remodeling and contractile dysfunction are leading causes in hypertrophy-associated heart failure (HF), increasing with a population’s rising age. A hallmark of aged and diseased hearts is the accumulation of modified proteins caused by an impaired autophagy-lysosomal-pathway. Although, autophagy inducer rapamycin has been described to exert cardioprotective effects, it remains to be shown whether these effects can be attributed to improved cardiomyocyte autophagy and contractility. In vivo hypertrophy was induced by transverse aortic constriction (TAC), with mice receiving daily rapamycin injections beginning six weeks after surgery for four weeks. Echocardiographic analysis demonstrated TAC-induced HF and protein analyses showed abundance of modified proteins in TAC-hearts after 10 weeks, both reduced by rapamycin. In vitro, cardiomyocyte hypertrophy was mimicked by endothelin 1 (ET-1) and autophagy manipulated by silencing Atg5 in neonatal cardiomyocytes. ET-1 and siAtg5 decreased Atg5–Atg12 and LC3-II, increased natriuretic peptides, and decreased amplitude and early phase of contraction in cardiomyocytes, the latter two evaluated using ImageJ macro Myocyter recently developed by us. ET-1 further decreased cell contractility in control but not in siAtg5 cells. In conclusion, ET-1 decreased autophagy and cardiomyocyte contractility, in line with siAtg5-treated cells and the results of TAC-mice demonstrating a crucial role for autophagy in cardiomyocyte contractility and cardiac performance. Full article
(This article belongs to the Special Issue Vascular Autophagy in Health and Disease)
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Review

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24 pages, 2403 KiB  
Review
Selective Autophagy in Hyperglycemia-Induced Microvascular and Macrovascular Diseases
by Leena P. Bharath, Jack Donato Rockhold and Rachel Conway
Cells 2021, 10(8), 2114; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10082114 - 17 Aug 2021
Cited by 17 | Viewed by 4297
Abstract
Dysregulation of autophagy is an important underlying cause in the onset and progression of many metabolic diseases, including diabetes. Studies in animal models and humans show that impairment in the removal and the recycling of organelles, in particular, contributes to cellular damage, functional [...] Read more.
Dysregulation of autophagy is an important underlying cause in the onset and progression of many metabolic diseases, including diabetes. Studies in animal models and humans show that impairment in the removal and the recycling of organelles, in particular, contributes to cellular damage, functional failure, and the onset of metabolic diseases. Interestingly, in certain contexts, inhibition of autophagy can be protective. While the inability to upregulate autophagy can play a critical role in the development of diseases, excessive autophagy can also be detrimental, making autophagy an intricately regulated process, the altering of which can adversely affect organismal health. Autophagy is indispensable for maintaining normal cardiac and vascular structure and function. Patients with diabetes are at a higher risk of developing and dying from vascular complications. Autophagy dysregulation is associated with the development of heart failure, many forms of cardiomyopathy, atherosclerosis, myocardial infarction, and microvascular complications in diabetic patients. Here, we review the recent findings on selective autophagy in hyperglycemia and diabetes-associated microvascular and macrovascular complications. Full article
(This article belongs to the Special Issue Vascular Autophagy in Health and Disease)
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21 pages, 1475 KiB  
Review
Beyond Self-Recycling: Cell-Specific Role of Autophagy in Atherosclerosis
by James M. Henderson, Christian Weber and Donato Santovito
Cells 2021, 10(3), 625; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10030625 - 11 Mar 2021
Cited by 21 | Viewed by 4484
Abstract
Atherosclerosis is a chronic inflammatory disease of the arterial vessel wall and underlies the development of cardiovascular diseases, such as myocardial infarction and ischemic stroke. As such, atherosclerosis stands as the leading cause of death and disability worldwide and intensive scientific efforts are [...] Read more.
Atherosclerosis is a chronic inflammatory disease of the arterial vessel wall and underlies the development of cardiovascular diseases, such as myocardial infarction and ischemic stroke. As such, atherosclerosis stands as the leading cause of death and disability worldwide and intensive scientific efforts are made to investigate its complex pathophysiology, which involves the deregulation of crucial intracellular pathways and intricate interactions between diverse cell types. A growing body of evidence, including in vitro and in vivo studies involving cell-specific deletion of autophagy-related genes (ATGs), has unveiled the mechanistic relevance of cell-specific (endothelial, smooth-muscle, and myeloid cells) defective autophagy in the processes of atherogenesis. In this review, we underscore the recent insights on autophagy’s cell-type-dependent role in atherosclerosis development and progression, featuring the relevance of canonical catabolic functions and emerging noncanonical mechanisms, and highlighting the potential therapeutic implications for prevention and treatment of atherosclerosis and its complications. Full article
(This article belongs to the Special Issue Vascular Autophagy in Health and Disease)
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17 pages, 1345 KiB  
Review
Autophagy and Mitophagy as Essential Components of Atherosclerosis
by Anastasia V. Poznyak, Nikita G. Nikiforov, Wei-Kai Wu, Tatiana V. Kirichenko and Alexander N. Orekhov
Cells 2021, 10(2), 443; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10020443 - 19 Feb 2021
Cited by 28 | Viewed by 4289
Abstract
Cardiovascular disease (CVD) is one of the greatest health problems affecting people worldwide. Atherosclerosis, in turn, is one of the most common causes of cardiovascular disease. Due to the high mortality rate from cardiovascular diseases, prevention and treatment at the earliest stages become [...] Read more.
Cardiovascular disease (CVD) is one of the greatest health problems affecting people worldwide. Atherosclerosis, in turn, is one of the most common causes of cardiovascular disease. Due to the high mortality rate from cardiovascular diseases, prevention and treatment at the earliest stages become especially important. This requires developing a deep understanding of the mechanisms underlying the development of atherosclerosis. It is well-known that atherogenesis is a complex multi-component process that includes lipid metabolism disorders, inflammation, oxidative stress, autophagy disorders and mitochondrial dysfunction. Autophagy is a cellular control mechanism that is critical to maintaining health and survival. One of the specific forms of autophagy is mitophagy, which aims to control and remove defective mitochondria from the cell. Particularly defective mitophagy has been shown to be associated with atherogenesis. In this review, we consider the role of autophagy, focusing on a special type of it—mitophagy—in the context of its role in the development of atherosclerosis. Full article
(This article belongs to the Special Issue Vascular Autophagy in Health and Disease)
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