Endothelial Dysfunction in Cardiovascular Diseases: The Role of Oxidative Stress

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 2404

Special Issue Editor


E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, Federal University of Paraíba, João Pessoa 58000-000, PB, Brazil
Interests: redox signaling, antioxidants, cardiovascular diseases, hypertension, endothelial dysfunction, natural products, aging, pulmonary hypertension

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. CVDs are linked to a number of risk factors, including smoking, high cholesterol, and high blood glucose levels. CVDs include hypertension, stroke, heart failure, and myocardial infarction, among others. The endothelium plays a major role in cardiovascular physiology. At the cellular level, endothelial dysfunction is a critical factor in the development of CVDs. Endothelial dysfunction also appears to be involved in the early stages of CVDs, including age-related CVDs. Aging-related changes to the heart and blood vessels may increase a person's risk of developing CVDs. Furthermore, aging can lead to CVDs, and as global life expectancy rises so will the prevalence of CVDs. Surprisingly, oxidative stress has been linked to endothelial dysfunction, aging-related endothelial dysfunction, and various CVDs.

ROS (reactive oxygen species) are a pleiotropic class of compounds with a wide range of oxidized properties that affect many genes and proteins at the physiological level. This signaling can be disrupted, resulting in cellular dysfunction and illness. Although oxidative stress and endothelial dysfunction are typically found in hypertensive individuals, new evidence suggests that they may play a causal role in the molecular mechanisms that contribute to hypertension. Substances that modulate redox signaling, reduce or attenuate oxidative stress, and target antioxidant genes, enzymes, and transcription factors are therefore essential for preventing or treating CVDs in both young and older people. Furthermore, recent studies demonstrate that endothelial dysfunction and injury in the vascular wall can be repaired by endothelial progenitor cells.

As a result of the above, this Special Issue welcomes original research papers or review articles focusing on the primary mechanisms underlying oxidative stress and how it leads to endothelial dysfunction and CVDs, as well as the beneficial role that natural products may play in endothelial dysfunction-related CVDs.

Prof. Dr. Isac Almeida de Medeiros
Guest Editor

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. Antioxidants 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 2900 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 progenitor cells
  • cardiovascular diseases
  • aging
  • oxidative stress
  • redox signaling
  • dna damage
  • hypertension
  • antioxidant system
  • natural products

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

13 pages, 460 KiB  
Review
Dicarbonyl-Dependent Modification of LDL as a Key Factor of Endothelial Dysfunction and Atherosclerotic Vascular Wall Damage
by Vadim Z. Lankin, Alla K. Tikhaze and Arthur M. Melkumyants
Antioxidants 2022, 11(8), 1565; https://doi.org/10.3390/antiox11081565 - 12 Aug 2022
Cited by 11 | Viewed by 1783
Abstract
The review presents evidence that the main damage to the vascular wall occurs not from the action of “oxidized” LDL, which contain hydroperoxy acyls in the phospholipids located in their outer layer, but from the action of LDL particles whose apoprotein B-100 is [...] Read more.
The review presents evidence that the main damage to the vascular wall occurs not from the action of “oxidized” LDL, which contain hydroperoxy acyls in the phospholipids located in their outer layer, but from the action of LDL particles whose apoprotein B-100 is chemically modified with low molecular weight dicarbonyls, such as malondialdehyde, glyoxal, and methylglyoxal. It has been argued that dicarbonyl-modified LDL, which have the highest cholesterol content, are particularly “atherogenic”. High levels of dicarbonyl-modified LDL have been found to be characteristic of some mutations of apoprotein B-100. Based on the reviewed data, we hypothesized a common molecular mechanism underlying vascular wall damage in atherosclerosis and diabetes mellitus. The important role of oxidatively modified LDL in endothelial dysfunction is discussed in detail. In particular, the role of the interaction of the endothelial receptor LOX-1 with oxidatively modified LDL, which leads to the expression of NADPH oxidase, which in turn generates superoxide anion radical, is discussed. Such hyperproduction of ROS can cause destruction of the glycocalyx, a protective layer of endotheliocytes, and stimulation of apoptosis in these cells. On the whole, the accumulated evidence suggests that carbonyl modification of apoprotein B-100 of LDL is a key factor responsible for vascular wall damage leading to atherogenesis and endothelial dysfunction. Possible ways of pharmacological correction of free radical processes in atherogenesis and diabetogenesis are also discussed. Full article
Show Figures

Figure 1

Back to TopTop