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Biomedicines
Special Issues
Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches 2.0
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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: 30 April 2025 | Viewed by 8504

Special Issue Editors

Dr. Byeong Hwa Jeon

E-Mail Website
Guest Editor
Department of Physiology, Chungnam National University, Daejeon, Republic of Korea
Interests: reactive oxygen species; vascular inflammation; endothelial dysfunction; biomaterials; tumor microenvironments
Special Issues, Collections and Topics in MDPI journals
Dr. Hee Kyoung Joo

E-Mail Website
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

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • 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 (4 papers)

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Research

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22 pages, 5813 KiB  
Article
Intracellular Iron Deficiency and Abnormal Metabolism, Not Ferroptosis, Contributes to Homocysteine-Induced Vascular Endothelial Cell Death
by Wenting Shi, Jing Zhang, Wairong Zhao, Meiyan Yue, Jie Ma, Silu Zeng, Jingyi Tang, Yu Wang and Zhongyan Zhou
Biomedicines 2024, 12(10), 2301; https://doi.org/10.3390/biomedicines12102301 - 10 Oct 2024
Viewed by 959
Abstract
Background/Objectives: Homocysteine (Hcy) and iron are factors co-related with the progression of cardiovascular diseases. The vascular endothelium is an important barrier for physiological homeostasis, and its impairment initiates cardiovascular injury. However, the mechanism underlying Hcy-caused vascular endothelial cell injury and the participation of [...] Read more.
Background/Objectives: Homocysteine (Hcy) and iron are factors co-related with the progression of cardiovascular diseases. The vascular endothelium is an important barrier for physiological homeostasis, and its impairment initiates cardiovascular injury. However, the mechanism underlying Hcy-caused vascular endothelial cell injury and the participation of iron are not fully elucidated. This study aims to investigate the Hcy-induced vascular endothelial injury and iron metabolism dysfunction as well as the underlying molecular mechanism. Methods: Human umbilical vein endothelial cells (HUVECs) were employed as the experimental model to examine the Hcy-induced endothelial injury and its underlying mechanism via various biochemical assays. Results: Hcy suppressed the cell viability and proliferation and caused cell death in a concentration-dependent manner. Hcy induced cell cycle arrest, apoptosis, and autophagy as well as impairment of intracellular energy metabolism. Hcy disrupted the intracellular antioxidant system and mitochondrial function by increasing intracellular ROS, MDA and mitochondrial content, and decreasing the SOD activity and mitochondrial membrane potential. Hcy significantly reduced the GSH-Px activity along with the accumulation of intracellular GSH in a concentration-dependent manner. Ferroptosis inhibitors, Ferrostatin-1 (Fer-1), and Deferoxamine (DFO) significantly decreased the Hcy-caused cytotoxicity accompanied by a reduction in dysregulated mitochondria content, but only DFO ameliorated the elevation of intracellular ROS, and neither Fer-1 nor DFO affected the Hcy-caused reduction in intracellular ATP. In addition, Hcy decreased the intracellular concentration of iron, and supplementing Hcy with various concentrations of Fe3+ increased the cell viability and decreased the LDH release in a concentration-dependent manner. Hcy dramatically decreased the mRNA expression level of transferrin receptor while increasing the mRNA expression levels of transferrin, ferritin light chain, ferritin heavy chain, ferroportin, and SLC7A11. Moreover, Hcy suppressed the protein expression of phospho-Akt, phospho-mTOR, Beclin-1, LC3A/B, Nrf2, HO-1, phospho-MEK1/2, phospho-ERK1/2, and Caspase-3 in concentration- and time-dependent manners. Conclusions: Hcy-induced vascular endothelial injury is likely to be associated with apoptosis and autophagy, but not ferroptosis. The key underlying mechanisms are involved in the disruption of the intracellular antioxidant system and iron metabolism via regulation of PI3K/Akt/mTOR, MAPKs, Nrf2/HO-1, and iron metabolism. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches 2.0)
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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 2436
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
(This article belongs to the Special Issue Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches 2.0)
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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
Cited by 2 | Viewed by 1738
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
(This article belongs to the Special Issue Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches 2.0)
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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 9 | Viewed by 2403
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
(This article belongs to the Special Issue Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches 2.0)
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