A special issue of Vessel Plus
ISSN 2574-1209 (Online)
Submission deadline: 30 Nov 2018
Articles of special issue are free of charge for article processing.
For Author Instructions, please refer to http://vpjournal.net/pages/view/author_instructions
For Online Submission, please login at http://www.oaemesas.com/vp
Submission Deadline: 30 Nov 2018
Contacts: Magge Ma, Managing Editor, editorialoffice@vpjournal.net
The following list shows the information of planned papers to this special issue. All the papers submitted to Vessel Plus will go through a rigorous peer review. (Please note that the information below is provisional and may be subject to future change)
Type of paper: Review article
Tentative Title: Dysfunctional HDL and Atherogenesis
Authors: Constantine E. Kosmas1, Delia Silverio2, Andreas Sourlas3, Frank Garcia2, Peter D. Montan2, Eliscer Guzman3
Affiliation: 1Department of Medicine, Division of Cardiology, Mount Sinai Hospital, New York, NY, USA; 2Cardiology Clinic, Cardiology Unlimited, PC, New York, NY, USA; 3School of Medicine, University of Crete, Heraklion, Greece; 4Department of Medicine, Division of Cardiology, Montefiore Medical Center, Bronx, NY, USA.
Possible Abstract:
HDL plays a major role in reverse cholesterol transport (RCT) but also exhibits antioxidative, anti-inflammatory endothelial/vasodilatory, antithrombotic and cytoprotective functions, which enhance its protective effect against cardiovascular disease (CVD). However, the function of HDL is dependent upon genetic, environmental and lifestyle factors. Modification of the protein components of HDL in several disease states may convert HDL from an anti-inflammatory to a proinflammatory and pro-atherogenic particle by limiting its ability to promote RCT and to prevent LDL modification. In our review, we will discuss the clinical and scientific data pertaining to the factors and conditions that impair HDL functionality and render HDL pro-atherogenic.
Type of paper: Review article
Tentative Title: Dyslipidemia and Atherosclerotic Carotid Artery Stenosis
Authors: Yoichi Miura, Hidenori Suzuki
Affiliation: Department of Neurosurgery, Mie University Graduate School of Medicine
Possible Abstract:
Carotid artery atherosclerosis or stenosis is frequently present at the carotid bifurcation or the internal carotid artery, accounting for at least 20% of all ischemic strokes. High levels of serum total cholesterol and low-density lipoprotein cholesterol are established risk factors for genesis and progression of atherosclerotic lesions through various mechanisms. In addition, accumulating evidence has shown that a high level of triglyceride is associated with increased atherosclerosis risks. So-called ‘vulnerable plaque’ with a large lipid core, thin fibrous cap and intraplaque hemorrhage tends to cause subsequent thromboembolic ischemic events. Statins are known not only to lower serum cholesterol levels but also to promote plaque stabilization via pleiotropic effects such as reducing subclinical systemic inflammation, endothelial activation, leukocyte intraplaque infiltration, and increasing intimal smooth muscle cell migration. This article discusses the mechanism of atherosclerosis formation induced by dyslipidemia, and the role of lipid-lowering agents including statins in patients with symptomatic and asymptomatic atherosclerotic carotid artery stenosis.
Type of paper: Review article
Tentative Title: Vascular Ion Channels in Atherogenesis
Authors: Ibra S. Fancher, Irena Levitan
Affiliation: Department of Medicine, Division of Pulmonary, Critical Care, Sleep and Allergy, University of Chicago at Illinois
Possible Abstract:
Remarkable advancements in our understanding of the pathological mechanisms of atherosclerosis have occurred over the last decade yet clinical targets for treating atherogenesis are still premature. Vascular ion channels are critically involved in a variety of cell processes that may promote or prevent atherogenesis including transducing mechanical signals and regulating cell proliferation and motility. Furthermore, several ion channels are directly modulated by sterols and fatty acids suggesting that vascular ion channels may be crucial to the initial processes in foam cell generation and lesion formation. Therefore, identifying specific ion channels involved in atherogenesis may provide clinical benefit if pro-athero channel activity can be blocked and anti-athero channel activity can be activated or prevented from being inhibited by disease processes. This review covers the existing literature to date on the various roles of ion channels in vascular cells driving atherogenesis.