Special Issue "Atherosclerosis: Molecular Mechanisms and Therapeutic Advances"

A special issue of J (ISSN 2571-8800).

Deadline for manuscript submissions: closed (15 October 2018).

Special Issue Editors

Prof. Dr. Maria Luisa Balestrieri
Website
Guest Editor
Department of Precision Medicine, School of Medicine, University of Campania “Luigi Vanvitelli”, Naples, Italy
Interests: aging; oxidative stress; nitric oxide; endothelial cells; endothelial progenitor cells; angiogenesis; inflammation; cell senescence; apoptosis; atherosclerosis; diabetes; endothelial dysfunction; sirtuins and cardiovascular disease; natural products; betaines; health; bioactive compounds; free radicals; antioxidants; ergothioneine; cell cycle; cancer-related biochemical pathways; cell proliferation; senescence; cancer cell death; epigenetic regulation; sirtuins and cancer
Special Issues and Collections in MDPI journals
Dr. Nunzia D'Onofrio
Website1 Website2
Guest Editor
Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, Naples, Italy
Interests: oxidative stress; endothelial cells; endothelial progenitor cells; endothelial dysfunction; inflammation; cell senescence; atherosclerosis; diabetes; sirtuins and cardiovascular disease; natural products; betaines; bioactive compounds; free radicals; antioxidants; ergothioneine

Special Issue Information

Dear Colleagues,

The development of atherosclerosis, a complex multifactorial process, is, at least in part, controlled by the functional state of the vascular endothelium, influenced by a broad set of cardiovascular risk factors. Hypercholesterolemia, hypertension, and diabetes mellitus enhance reactive oxygen species  generation, resulting in oxidative modification of lipoproteins and phospholipids, all mechanisms that contribute to atherogenesis. A pivotal role for inflammation in the pathogenesis of atherosclerosis has been recognized and proved at molecular levels. However, despite current knowledge, results coming from genome wide association studies are expected to uncover the complex inflammatory process subtending atherosclerosis, thus opening a new scenario for  tailored target therapy. Moreover, several pieces of evidence point towards the crosstalk between long non-coding RNAs and vasculature in regulating the development of vessel lining and recruitment of immune cells, such as macrophages, at the site of injury and inflammation. In particular, the modulation of atherosclerosis by long non-coding RNAs has brought significant attention over the past few years. This Special Issue welcomes both original papers and review articles addressing one or several of the above-mentioned issues, or of the topics mentioned in the keywords listed below.

Prof. Dr. Maria Luisa Balestrieri
Dr. Nunzia D'Onofrio
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 papers will be 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. J is an international peer-reviewed open access quarterly 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 1000 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
  • Arterial Disease
  • Atherosclerosis
  • Atherosclerotic plaque
  • Vascular diseases
  • Inflammation
  • Reactive oxygen species
  • Oxidative stress
  • Nitric oxide
  • Long non-coding RNAs
  • Whole-genome sequencing
  • Genetics, Anti-inflammatory drugs
  • Genome wide association study
  • DNA sequencing

Published Papers (2 papers)

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Review

Open AccessReview
Inflammation and Peripheral Arterial Disease
J 2019, 2(2), 142-151; https://doi.org/10.3390/j2020012 - 03 Apr 2019
Abstract
Peripheral arterial disease (PAD) is an atherosclerotic disease closely associated with high morbidity and mortality in cardiac events. Inflammation is crucial in atherosclerosis both at triggering and in progression. Numerous inflammatory biomarkers (cytokines, matrix metalloproteinases (MMPs), selectin, intracellular adhesion molecule (ICAM), vascular cell [...] Read more.
Peripheral arterial disease (PAD) is an atherosclerotic disease closely associated with high morbidity and mortality in cardiac events. Inflammation is crucial in atherosclerosis both at triggering and in progression. Numerous inflammatory biomarkers (cytokines, matrix metalloproteinases (MMPs), selectin, intracellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) C-reactive protein (CRP), fibrinogen) have been measured in atherosclerotic diseases including PAD. This paper summarizes the data on the inflammatory biomarkers for PAD pathophysiology and highlights the most useful markers in monitoring PAD outcomes. Full article
(This article belongs to the Special Issue Atherosclerosis: Molecular Mechanisms and Therapeutic Advances)
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Open AccessReview
Emerging Roles of Cardiotrophin-1 in the Pathogenesis and Biomarker of Atherosclerosis
J 2018, 1(1), 94-105; https://doi.org/10.3390/j1010010 - 20 Sep 2018
Cited by 2
Abstract
Cardiotrophin-1 (CT-1), an interleukin-6 family cytokine, is known as an active inducer capable of cardiac hypertrophy and vascular stiffness in hypertensive heart disease. CT-1 is expressed at high levels in the heart, vascular endothelial cells (ECs), and adipocytes. CT-1 stimulates inflammatory and proatherogenic [...] Read more.
Cardiotrophin-1 (CT-1), an interleukin-6 family cytokine, is known as an active inducer capable of cardiac hypertrophy and vascular stiffness in hypertensive heart disease. CT-1 is expressed at high levels in the heart, vascular endothelial cells (ECs), and adipocytes. CT-1 stimulates inflammatory and proatherogenic molecule expression in human monocytes and ECs, as well as monocyte-EC adhesion. CT-1 enhances oxidized low-density lipoprotein-induced foam-cell formation in human monocyte-derived macrophages. CT-1 stimulates the migration, proliferation, and colloagen-1 production in human vascular smooth muscle cells. Chronic CT-1 infusion into Apoe−/− mice accelerates the development of aortic atherosclerotic lesions. CT-1 is expressed at high levels in ECs and macrophage foam cells within atheromatous plaques in Apoe−/− mice. A blockade of CT-1 using anti-CT-1 neutralizing antibody results in the prevention of atherogenesis in Apoe−/− mice. Plasma CT-1 concentrations are elevated in patients with hypertensive heart disease, ischemic heart disease, and metabolic syndrome, and are positively associated with the severity of cardiac hypertrophy, heart failure, and atherosclerosis. Increased plasma concentration of CT-1 is a predictor of death and heart failure following acute myocardial infarction. Therefore, CT-1 serves a novel therapeutic target for atherosclerosis and related diseases. Plasma CT-1 may be a reliable biomarker for atherosclerotic cardiovascular diseases. Full article
(This article belongs to the Special Issue Atherosclerosis: Molecular Mechanisms and Therapeutic Advances)
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