Special Issue "Atherosclerosis: Molecular Mechanisms and Therapeutic Advances"
A special issue of J (ISSN 2571-8800).
Deadline for manuscript submissions: closed (15 October 2018).
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
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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
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
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 1200 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.
- Endothelial dysfunction
- Arterial Disease
- Atherosclerotic plaque
- Vascular diseases
- Reactive oxygen species
- Oxidative stress
- Nitric oxide
- Long non-coding RNAs
- Whole-genome sequencing
- Genetics, Anti-inflammatory drugs
- Genome wide association study
- DNA sequencing