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Special Issue "Lipids in Health and Disease"

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 31 March 2020

Special Issue Editor

Guest Editor
Dr. Pierluigi Plastina

Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy
Website | E-Mail
Interests: antioxidants; bioactive lipids; cancer; inflammation; phenolipids

Special Issue Information

Dear Colleagues,

Over the past several decades, our perception of lipids has dramatically changed. They are no longer considered as mere energy sources or constituents of cell membranes but rather, it is now clear that they play an essential role in physiology and pathophysiology. Lipids act as messengers in inflammation and immunity and are crucial in migration, apoptosis, autophagy, and cell division. Some of them have become extremely popular to the majority of people, as in the case of omega-3 polyunsaturated fatty acids (PUFAs) or phytosterols whose beneficial properties are recognized for certain (patho)physiological conditions. This Special Issue is aimed to cover new advances in lipid action in health and disease, with particular focus on: (a) lipid effects and underlying mechanisms in cardiovascular, neurological, and metabolic diseases, as well as in aging, immunity, inflammation, and cancer; (b) synthesis and properties of structured lipids and phenolipids; (c) new approaches in the metabolic profiling of lipids; (d) lipid peroxidation in biological systems.

Dr. Pierluigi Plastina
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 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. Molecules is an international peer-reviewed open access semimonthly 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 1800 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

  • Endocannabinoids
  • Essential fatty acids
  • Lipid peroxidation
  • Lipidomics
  • Lipids
  • Lipoproteins
  • Omega-3 PUFAs
  • Phenolipids
  • Phospolipids
  • Sterols
  • Structured lipids
  • Vitamins and provitamins

Published Papers (1 paper)

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Research

Open AccessArticle
Simvastatin Attenuates H2O2-Induced Endothelial Cell Dysfunction by Reducing Endoplasmic Reticulum Stress
Molecules 2019, 24(9), 1782; https://doi.org/10.3390/molecules24091782
Received: 13 April 2019 / Revised: 7 May 2019 / Accepted: 8 May 2019 / Published: 8 May 2019
PDF Full-text (2683 KB) | HTML Full-text | XML Full-text
Abstract
Atherosclerosis is the pathological basis of cardiovascular disease, whilst endothelial dysfunction (ED) plays a primary role in the occurrence and development of atherosclerosis. Simvastatin has been shown to possess significant anti-atherosclerosis activity. In this study, we evaluated the protective effect of simvastatin on [...] Read more.
Atherosclerosis is the pathological basis of cardiovascular disease, whilst endothelial dysfunction (ED) plays a primary role in the occurrence and development of atherosclerosis. Simvastatin has been shown to possess significant anti-atherosclerosis activity. In this study, we evaluated the protective effect of simvastatin on endothelial cells under oxidative stress and elucidated its underlying mechanisms. Simvastatin was found to attenuate H2O2-induced human umbilical vein endothelial cells (HUVECs) dysfunction and inhibit the Wnt/β-catenin pathway; however, when this pathway was activated by lithium chloride, endothelial dysfunction was clearly enhanced. Further investigation revealed that simvastatin did not alter the expression or phosphorylation of LRP6, but reduced intracellular cholesterol deposition and inhibited endoplasmic reticulum (ER) stress. Inducing ER stress with tunicamycin activated the Wnt/β-catenin pathway, whereas reducing ER stress with 4-phenylbutyric acid inhibited it. We hypothesize that simvastatin does not affect transmembrane signal transduction in the Wnt/β-catenin pathway, but inhibits ER stress by reducing intracellular cholesterol accumulation, which blocks intracellular signal transduction in the Wnt/β-catenin pathway and ameliorates endothelial dysfunction. Full article
(This article belongs to the Special Issue Lipids in Health and Disease)
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