Guest Editor(s)

• Prof. Maurizio Averna

  Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), School of Medicine, University of Palermo, Palermo, Italy.

  Website | E-mail

Special Issue Introduction

Atherosclerosis is a chronic inflammatory disorder of the arterial wall. The progression of the atherosclerotic plaque to advanced lesion leads to erosion, rupture and thrombotic events. In the advanced lesions, several cell types are involved including macrophages, smooth muscle cells, T-cells and dendritic cells, indicating that besides the cholesterol accumulation, an active immune-inflammatory response is going on. The inflammasome activation represents the molecular check point that links cholesterol accumulation to inflammation in each phase of atherosclerosis, from plaque formation to acute coronary syndromes. Metabolic conditions have been shown to contribute to the progression of atherosclerosis also through inflammatory mechanisms. First, an alteration in lipid metabolism such as the Hypercholesterolemia. Local endothelial dysfunction leads to the retention in the arterial wall of LDLs that facilitate the recruitment of circulating monocytes and immune cells and activate the immune-inflammatory response in the atherosclerotic plaque once oxidized. The Metabolic Syndrome has been associated with an increased risk of atherosclerotic cardiovascular events; the increase production of inflammatory and oxidative stress mediators, i.e. adipokines and ROS, represents a link among Metabolic Syndrome, inflammation and atherogenesis. Diabetes is associated with an accelerated development of atherosclerosis that may be due to many contributors such as atherogenic LDL, hyperglycemia, oxidative stress, and increased inflammation. Altered Uric acid metabolism has been linked to an increased risk of atherosclerosis and cardiovascular events. Uric acid is a potent antioxidant but it also plays a role of oxidant. Many lines of evidences seem to suggest a role of uric acid in the endothelial activation and in the increased risk of coronary artery disease.

The scope of this special issue is to provide a comprehensive and updated view of the molecular pathways as well as the clinical correlations that underlie the interplay among some common and prevalent metabolic conditions, inflammation and atherosclerosis. It will focus on the general mechanisms of immune-inflammation in atherosclerosis and on the role of hypercholesterolemia, metabolic syndrome, diabetes and uric acid metabolism.

Keywords

Atherosclerosis, inflammation, metabolic disease, hypercholesterolemia, diabetes, metabolic syndrome, uric acid

Submission Deadline

15 Dec 2020

Submission Information

For Author Instructions, please refer to http://vpjournal.net/pages/view/author_instructions
For Online Submission, please login at https://oaemesas.com/login?JournalId=vp&SpecialIssueId=488
Submission Deadline: 15 Dec 2020
Contacts: Alisa Wang, Assistant Editor, alisa@vpjournal.net

Planned Papers

Type: Review

Title: Metabolic syndrome and atherosclerosis: the role of oxidative stress and inflammation

Authors: Eugenia Hopps

Affiliations: Department of Emergency Medicine, University Hospital of Palermo ia del Vespro, Palermo 129 - 90127, Italy.

Abstract: Metabolic syndrome (MS), which involves factors as obesity, insulin resistance, diabetes mellitus, arterial hypertension and dyslipidemia, is commonly accompanied by an elevated cardiovascular risk with high morbidity and mortality. The alterations of the arterial vasculature begin with the endothelial dysfunction and lead to micro- and macrovascular complications. The remodelling of the endothelial basal membrane, which promotes erosion and thrombosis, has a multifactorial pathogenesis that includes leukocyte activation, subclinical inflammation, increased reactive oxygen species (ROS) production, and also an altered matrix metalloproteinases (MMPs) expression.
A strong association between MS and an altered oxidant/antioxidant status has been demonstrated. In case of endothelial dysfunction, the superoxide anion oxidizes nitric oxide (NO) reducing its availability and starting a cascade of ROS generation that leads to the oxidation of carbohydrates, proteins and lipids. Oxidized low-density lipoproteins (oxLDLs) are often increased in newly diagnosed MS subjects.
MMPs are endopeptidases degrading extracellular matrix proteins, which are involved in the atherosclerotic lesion development and progression and could be implicated in plaque instability. In MS an impaired MMP expression has been demonstrated and it is associated with a higher risk of all-cause and cardiovascular mortality.
Chronic systemic inflammation is a common feature of MS, and it is mostly induced by the release of inflammatory molecules (IL-6, TNF-α, leptin, adiponectin, resistin) in the visceral adipose tissue. The proinflammatory status seems to be the link between oxidative stress and MMP profile in MS and it contributes to the plaque development influencing the activity of endothelial cells, macrophages and vascular smooth muscle cells.

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