Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 6880

Special Issue Editors


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Guest Editor
Department of Physiology, Chungnam National University, Daejeon, Republic of Korea
Interests: reactive oxygen species; vascular inflammation; endothelial dysfunction; biomaterials; tumor microenvironments
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Guest Editor
1. Research Institute for Medical Sciences, College of Medicine, Chungnam National University, 266 Munhwa-ro, Jung-gu, Daejeon 35015, Republic of Korea
2. Department of Physiology, College of Medicine, Chungnam National University, 266 Munhwa-ro, Jung-gu, Daejeon 35015, Republic of Korea
Interests: aortic inflammation; vascular inflammation; endothelial activation

Special Issue Information

Dear Colleagues,

The Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches 2.0”, will focus on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions related to vascular inflammation.

Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. The chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment.

The pathophysiology of endothelial dysfunction (ED) is complex, and multifactorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions as well as the early detection or molecular imaging techniques for endothelial dysfunction help to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had a promising beneficial effect in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune responses near tumor environments.

This Special Issue is open for a wide range of basic to preclinical research studies, or those adopting a multidisciplinary approach, and will also cover original articles and reviews on the following topics:

  • Target molecules or pathophysiology
  • Primary prevention of cardiovascular risk factors
  • Early detection or molecular imaging techniques
  • New therapeutic approaches including biomaterials development
  • Drug delivery systems
  • Immunology and tumor environments

Dr. Byeong Hwa Jeon
Dr. Hee Kyoung Joo
Guest Editors

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Keywords

  • endothelial dysfunction
  • endothelial activation
  • reactive oxygen species and lipid peroxidation
  • atherosclerosis
  • adipose tissues and obesity
  • hypertension
  • hypercholesterolemia
  • vascular inflammation
  • tumor microenvironment
  • new biomarker or pathophysiology
  • novel therapeutic approach and pharmaceuticals

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Related Special Issue

Published Papers (3 papers)

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Research

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12 pages, 2211 KiB  
Article
Capsanthin Inhibits Atherosclerotic Plaque Formation and Vascular Inflammation in ApoE−/− Mice
by Sungmin Kim, Yu-Ran Lee, Eun-Ok Lee, Hao Jin, Yeon-Hee Choi, Hee-Kyoung Joo and Byeong-Hwa Jeon
Biomedicines 2022, 10(8), 1780; https://doi.org/10.3390/biomedicines10081780 - 23 Jul 2022
Cited by 1 | Viewed by 2234
Abstract
Capsanthin is a red pigment and the major carotenoid component of red paprika (Capsicum annuum L.). However, its role in atherosclerosis is yet to be fully elucidated. This study investigated the role of dietary capsanthin in vascular inflammation in atherosclerotic mice. We [...] Read more.
Capsanthin is a red pigment and the major carotenoid component of red paprika (Capsicum annuum L.). However, its role in atherosclerosis is yet to be fully elucidated. This study investigated the role of dietary capsanthin in vascular inflammation in atherosclerotic mice. We evaluated the anti-atherosclerotic effects of daily oral administration of capsanthin (0.5 mg/kg of body weight/day) in apolipoprotein E-deficient (ApoE−/−) mice fed a Western-type diet (WD). Capsanthin treatment inhibited vascular cell adhesion molecule 1 expression and nuclear factor-κB ser536 phosphorylation in tumor necrosis factor-α-stimulated cultured endothelial cells. Dietary capsanthin significantly inhibited the WD-induced elevation in the plasma levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglyceride in mice. Interestingly, capsanthin reduced aortic plaque formation and VCAM-1 expression, which is vascular inflammation, in atherosclerotic mice. In addition, the neutrophil–lymphocyte ratio, a systemic inflammatory marker, was inhibited in capsanthin-treated mice. Furthermore, capsanthin significantly reduced the levels of proinflammatory cytokines, such as TNF-α, interleukin-6, and monocyte chemoattractant protein-1, in the plasma of atherosclerotic mice. Collectively, our data demonstrate that dietary capsanthin plays a protective role against atherosclerosis in hyperlipidemic mice. This protective effect could be attributed to the anti-inflammatory properties of capsanthin. Full article
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Review

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16 pages, 1069 KiB  
Review
Unraveling the Role of Endothelial Dysfunction in Osteonecrosis of the Femoral Head: A Pathway to New Therapies
by Wenkai Shao, Ping Wang, Xiao Lv, Bo Wang, Song Gong and Yong Feng
Biomedicines 2024, 12(3), 664; https://doi.org/10.3390/biomedicines12030664 - 15 Mar 2024
Viewed by 1377
Abstract
Osteonecrosis of the femoral head (ONFH) is a disabling disease characterized by the disruption of the blood supply to the femoral head, leading to the apoptosis and necrosis of bone cells and subsequent joint collapse. Total hip arthroplasty is not optimal since most [...] Read more.
Osteonecrosis of the femoral head (ONFH) is a disabling disease characterized by the disruption of the blood supply to the femoral head, leading to the apoptosis and necrosis of bone cells and subsequent joint collapse. Total hip arthroplasty is not optimal since most patients are young. Multiple risk factors contribute to osteonecrosis, including glucocorticoid (GC) usage, excessive alcohol intake, hypercholesterolemia, and smoking. Continuous stimulation by many variables causes a chronic inflammatory milieu, with clinical repercussions including endothelial dysfunction, leading to thrombosis, coagulopathy, and poor angiogenesis. Immune cells are the primary regulators of inflammation. Innate and adaptive immune cells interact with endothelial cells to hinder the regeneration and repair of bone lesions. An in-depth examination of the pathological drivers of ONFH reveals that endothelial dysfunction may be a major cause of osteonecrosis. Understanding the involvement of endothelial dysfunction in the chronic inflammation of osteonecrosis could aid in the development of possible therapies. This review summarizes the role of endothelial cells in osteonecrosis and further explains the pathophysiological mechanism of endothelial dysfunction in this disease from the perspective of inflammation to provide new ideas for the treatment of osteonecrosis. Full article
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16 pages, 1051 KiB  
Review
The Role of Selenium in Atherosclerosis Development, Progression, Prevention and Treatment
by Siarhei A. Dabravolski, Vasily N. Sukhorukov, Alexandra A. Melnichenko, Victoria A. Khotina and Alexander N. Orekhov
Biomedicines 2023, 11(7), 2010; https://doi.org/10.3390/biomedicines11072010 - 17 Jul 2023
Cited by 8 | Viewed by 2069
Abstract
Selenium is an essential trace element that is essential for various metabolic processes, protection from oxidative stress and proper functioning of the cardiovascular system. Se deficiency has long been associated with multiple cardiovascular diseases, including endemic Keshan’s disease, common heart failure, coronary heart [...] Read more.
Selenium is an essential trace element that is essential for various metabolic processes, protection from oxidative stress and proper functioning of the cardiovascular system. Se deficiency has long been associated with multiple cardiovascular diseases, including endemic Keshan’s disease, common heart failure, coronary heart disease, myocardial infarction and atherosclerosis. Through selenoenzymes and selenoproteins, Se is involved in numerous crucial processes, such as redox homeostasis regulation, oxidative stress, calcium flux and thyroid hormone metabolism; an unbalanced Se supply may disrupt these processes. In this review, we focus on the importance of Se in cardiovascular health and provide updated information on the role of Se in specific processes involved in the development and pathogenesis of atherosclerosis (oxidative stress, inflammation, endothelial dysfunction, vascular calcification and vascular cell apoptosis). We also discuss recent randomised trials investigating Se supplementation as a potential therapeutic and preventive agent for atherosclerosis treatment. Full article
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