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Cells
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Novel Mechanisms Linking Metabolic Disorders and Cardiovascular Diseases
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Novel Mechanisms Linking Metabolic Disorders and Cardiovascular Diseases

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

Deadline for manuscript submissions: closed (20 December 2021) | Viewed by 9713

Special Issue Editors

Prof. Dr. Hong Wang

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Guest Editor
Centers for Metabolic Disease Research and Department of Cardiovascular Science, Temple University Lewis Katz School of Medicine, MERB Rm. 1060, 3500 North Broad Street, Philadelphia, PA, USA
Interests: cardiovascular diseases; hyperlipidemia; hyperhomocysteinemia; obesity; vascular inflammation; diabetes; stroke; chronic kidney disease
Dr. Hong Chen

E-Mail Website
Co-Guest Editor
Vascular Biology Program, Department of Surgery, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Interests: atherosclerosis; angiogenesis; diabetes; lymphatic disorders; obesity; vascular inflammation; hypertension; stroke; cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Jingyan Han

E-Mail Website
Co-Guest Editor
Vascular Biology Section/Department of Medicine, Whitaker Cardiovascular Research Institute, Boston University School of Medicine, #X725, 650 Albany Street, Boston, MA, 02118, USA
Interests: cardiovascular diseases; vascular endothelial dysfunction, redox biology, atherosclerosis, vascular aging, vascular impact of chronic alcohol binge drinking
Prof. Dr. Xiao-Feng Yang

E-Mail Website
Co-Guest Editor
Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA
Interests: vascular immunology and atherosclerosis; immunometabolism; epigenetic pathology

Special Issue Information

Although excellent achievements have been made in improving cardiovascular outcomes through effective prevention and treatment strategies, cardiovascular disease (CVD) remains the most common cause of death and disability worldwide. Persistence of metabolic CVD risk factors, such as hyperlipidemia, obesity, hyperhomocysteinemia and diabetic mellitus has been well recognized as the main causes for the prevalence of CVD. Therefore, there is a need to better understand the underlying mechanisms of the link between metabolic abnormalities and CVD, providing key insights into the pathogenesis of CVD associated with metabolic diseases that can lead to new therapeutic options. In line with our commitment to advance scientific understanding in cell biology and pathophysiology, Cells will publish a uniquely themed issue to present the progress of robust basic and translational research on this important area.           

In this Call for Papers, we welcome any manuscripts that address the novel molecular and cellular mechanisms that underscore the connection between metabolic diseases and CVD, as well as lymphedema and lymphatic disorders. The types of manuscripts include original experimental research review articles and comments (clinical and epidemiological studies may not be favorably reviewed). A wide range of topics will be considered as outlined below, but not limited to:

  • Metabolic diseases include dyslipidemia, hyperhomocysteinemia, type I and II diabetes, obesity, chronic kidney disease, as well as inherited metabolic disorders (e.g., lysosomal storage disorders, glycogen storage diseases, mitochondrial disorders)
  • Cardiovascular diseases include hypertension, coronary artery diseases (angina, myocardial infarction), stroke, heart failure, rheumatic heart disease, cardiomyopathy, atrial fibrillation and arrythmia, aortic aneurysms, peripheral artery disease, thromboembolic disease, and venous thrombosis
  • Cross-talks between signaling and metabolic reprogramming in heart and vasculature

Prof. Dr. Hong Wang
Guest Editor
Dr. Hong Chen
Dr. Jingyan Han
Prof. Dr. Xiao-Feng Yang
Co-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

  • cardiovascular disease
  • metabolic diseases
  • mechanisms

Published Papers (3 papers)

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Research

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20 pages, 6914 KiB  
Article
Neutrophil Elastase Increases Vascular Permeability and Leukocyte Transmigration in Cultured Endothelial Cells and Obese Mice
by Chinchu Jagadan Ushakumari, Qiong L. Zhou, Yu-Hua Wang, Sijia Na, Michael C. Rigor, Cindy Y. Zhou, Max K. Kroll, Benjamin D. Lin and Zhen Y. Jiang
Cells 2022, 11(15), 2288; https://doi.org/10.3390/cells11152288 - 25 Jul 2022
Cited by 10 | Viewed by 3278
Abstract
Neutrophil elastase (NE) plays a pivotal role in inflammation. However, the mechanism underlying NE-mediated inflammation in obesity remains unclear. Here, we report that NE activates protease-activated receptor-2 (PAR2), stimulates actin filament (F-actin) formation, decreases intercellular junction molecule VE-cadherin expression, and increases the permeability [...] Read more.
Neutrophil elastase (NE) plays a pivotal role in inflammation. However, the mechanism underlying NE-mediated inflammation in obesity remains unclear. Here, we report that NE activates protease-activated receptor-2 (PAR2), stimulates actin filament (F-actin) formation, decreases intercellular junction molecule VE-cadherin expression, and increases the permeability of human arterial endothelial cells (hECs). NE also prompts degradation of VE-cadherin and its binding proteins p120- and β-catenins via MG132-sensitive proteasomes. NE stimulates phosphorylation of myosin light-chain (MLC) and its regulator myosin phosphatase target subunit-1 (MYPT1), a target of Rho kinase (ROCK). Inhibitors of PAR2 and ROCK prohibit NE-induced F-actin formation, MLC phosphorylation, and VE-cadherin reduction in hECs, and impede monocyte transmigration through hEC monolayer pretreated with either neutrophils or NE. Further, administration of an NE inhibitor GW311616A significantly attenuates vascular leakage, leukocyte infiltration, and the expression of proinflammatory cytokines in the white adipose tissue from high-fat diet (HFD)-induced obese mice. Likewise, NE-deficient mice are resistant to HFD-induced vascular leakage in the heart. Together, NE regulates actomyosin cytoskeleton activity and VE-cadherin expression by activating PAR2 signaling in the endothelial cells, leading to increased vascular permeability and leukocyte extravasation. Hence, inhibition of NE is a potential approach to mitigate vascular injury and leukocyte infiltration in obesity-related systemic inflammation. Full article
(This article belongs to the Special Issue Novel Mechanisms Linking Metabolic Disorders and Cardiovascular Diseases)
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15 pages, 4822 KiB  
Article
Epsins Negatively Regulate Aortic Endothelial Cell Function by Augmenting Inflammatory Signaling
by Yunzhou Dong, Beibei Wang, Kui Cui, Xiaofeng Cai, Sudarshan Bhattacharjee, Scott Wong, Douglas B. Cowan and Hong Chen
Cells 2021, 10(8), 1918; https://doi.org/10.3390/cells10081918 - 29 Jul 2021
Cited by 3 | Viewed by 2774
Abstract
Background: The endothelial epsin 1 and 2 endocytic adaptor proteins play an important role in atherosclerosis by regulating the degradation of the calcium release channel inositol 1,4,5-trisphosphate receptor type 1 (IP3R1). In this study, we sought to identify additional targets responsible for epsin-mediated [...] Read more.
Background: The endothelial epsin 1 and 2 endocytic adaptor proteins play an important role in atherosclerosis by regulating the degradation of the calcium release channel inositol 1,4,5-trisphosphate receptor type 1 (IP3R1). In this study, we sought to identify additional targets responsible for epsin-mediated atherosclerotic endothelial cell activation and inflammation in vitro and in vivo. Methods: Atherosclerotic ApoE−/− mice and ApoE−/− mice with an endothelial cell-specific deletion of epsin 1 on a global epsin 2 knock-out background (EC-iDKO/ApoE−/−), and aortic endothelial cells isolated from these mice, were used to examine inflammatory signaling in the endothelium. Results: Inflammatory signaling was significantly abrogated by both acute (tumor necrosis factor-α (TNFα) or lipopolysaccharide (LPS)) and chronic (oxidized low-density lipoprotein (oxLDL)) stimuli in EC-iDKO/ApoE−/− mice and murine aortic endothelial cells (MAECs) isolated from epsin-deficient animals when compared to ApoE−/− controls. Mechanistically, the epsin ubiquitin interacting motif (UIM) bound to Toll-like receptors (TLR) 2 and 4 to potentiate inflammatory signaling and deletion of the epsin UIM mitigated this interaction. Conclusions: The epsin endocytic adaptor proteins potentiate endothelial cell activation in acute and chronic models of atherogenesis. These studies further implicate epsins as therapeutic targets for the treatment of inflammation of the endothelium associated with atherosclerosis. Full article
(This article belongs to the Special Issue Novel Mechanisms Linking Metabolic Disorders and Cardiovascular Diseases)
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Review

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17 pages, 1291 KiB  
Review
Adipocyte Phenotype Flexibility and Lipid Dysregulation
by Kyle J. Preston, Rosario G. Scalia and Michael V. Autieri
Cells 2022, 11(5), 882; https://doi.org/10.3390/cells11050882 - 3 Mar 2022
Cited by 6 | Viewed by 2976
Abstract
The prevalence of obesity and associated cardiometabolic diseases continues to rise, despite efforts to improve global health. The adipose tissue is now regarded as an endocrine organ since its multitude of secretions, lipids chief among them, regulate systemic functions. The loss of normal [...] Read more.
The prevalence of obesity and associated cardiometabolic diseases continues to rise, despite efforts to improve global health. The adipose tissue is now regarded as an endocrine organ since its multitude of secretions, lipids chief among them, regulate systemic functions. The loss of normal adipose tissue phenotypic flexibility, especially related to lipid homeostasis, appears to trigger cardiometabolic pathogenesis. The goal of this manuscript is to review lipid balance maintenance by the lean adipose tissue’s propensity for phenotype switching, obese adipose tissue’s narrower range of phenotype flexibility, and what initial factors account for the waning lipid regulatory capacity. Metabolic, hypoxic, and inflammatory factors contribute to the adipose tissue phenotype being made rigid. A better grasp of normal adipose tissue function provides the necessary context for recognizing the extent of obese adipose tissue dysfunction and gaining insight into how pathogenesis evolves. Full article
(This article belongs to the Special Issue Novel Mechanisms Linking Metabolic Disorders and Cardiovascular Diseases)
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