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Molecular Mechanisms and Pathophysiology of Atherosclerosis 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 7696

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Special Issue Editor

Dr. Noemí Rotllan

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Guest Editor

Institut dInvestigació Biomèdica Sant Pau (IIB Sant Pau), 08041 Barcelona, Spain
Interests: atherosclerosis; miRNAs; lipid metabolism; therapeutic approaches
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Several aspects contribute to plaque formation, such as lipid metabolism dysregulation, unbalanced cholesterol levels in the plasma, and the dysfunction and inflammation of the three key components of the arterial wall—endothelial cells, vascular smooth muscle cells, and macrophages. In the era of precision nanomedicine, significant efforts have been focused on the development of therapeutic tools capable of specifically directing treatment toward those key cells that play an important role during atheroma progression. Non-coding RNA has emerged as an important transcriptional and post-transcriptional regulator of target genes in several pathological diseases, including atherosclerosis, which is a major risk factor for cardiovascular disease and death. However, therapy with non-coding RNAs faces challenges, such as achieving tissue-specific, efficient, and safe delivery in vivo. Thus, for this Special Issue of IJMS, entitled “Molecular Mechanisms and Pathophysiology of Atherosclerosis”, we welcome the submission of original research and review papers on this widely discussed topic.

Dr. Noemí Rotllan
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 submissions that pass pre-check are 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

non-coding RNA
atherosclerosis
vascular biology
therapeutic approaches

Published Papers (4 papers)

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Research

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14 pages, 2380 KiB

Open AccessArticle

Haplotype of the Lipoprotein(a) Gene Variants rs10455872 and rs3798220 Is Associated with Parameters of Coagulation, Fibrinolysis, and Inflammation in Patients after Myocardial Infarction and Highly Elevated Lipoprotein(a) Values

by Sabina Ugovšek, Andreja Rehberger Likozar, Tina Levstek, Katarina Trebušak Podkrajšek, Janja Zupan and Miran Šebeštjen

Int. J. Mol. Sci. 2024, 25(2), 736; https://doi.org/10.3390/ijms25020736 - 06 Jan 2024

Viewed by 849

Abstract

Lipoprotein(a) (Lp(a)) is an independent risk factor for future coronary events. Variants rs10455872 and rs3798220 in the gene encoding Lp(a) are associated with an increased Lp(a) concentration and risk of coronary artery disease. We aimed to determine whether in high-risk coronary artery disease patients these two genetic variants and the kringle IV type 2 (KIV-2) repeats are associated with impairment of inflammatory and hemostatic parameters. Patients after myocardial infarction with elevated Lp(a) levels were included. Blood samples underwent biochemical and genetic analyses. In carriers of the AC haplotype, the concentrations of tumor necrosis factor (TNF)-α (4.46 vs. 3.91 ng/L, p = 0.046) and plasminogen activator inhibitor-1 (PAI-1) (p = 0.026) were significantly higher compared to non-carriers. The number of KIV-2 repeats was significantly associated with the concentration of high-sensitivity C-reactive protein (ρ = 0.251, p = 0.038) and overall fibrinolytic potential (r = −0.253, p = 0.038). In our patients, a direct association between the AC haplotype and both TNF-α and PAI-1 levels was observed. Our study shows that the number of KIV-2 repeats not only affects proatherosclerotic and proinflammatory effects of Lp(a) but is also associated with its antifibrinolytic properties. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Atherosclerosis 2.0)

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Review

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25 pages, 2713 KiB

Open AccessReview

The Evolving Role of Dendritic Cells in Atherosclerosis

by Simone Britsch, Harald Langer, Daniel Duerschmied and Tobias Becher

Int. J. Mol. Sci. 2024, 25(4), 2450; https://doi.org/10.3390/ijms25042450 - 19 Feb 2024

Viewed by 798

Abstract

Atherosclerosis, a major contributor to cardiovascular morbidity and mortality, is characterized by chronic inflammation of the arterial wall. This inflammatory process is initiated and maintained by both innate and adaptive immunity. Dendritic cells (DCs), which are antigen-presenting cells, play a crucial role in the development of atherosclerosis and consist of various subtypes with distinct functional abilities. Following the recognition and binding of antigens, DCs become potent activators of cellular responses, bridging the innate and adaptive immune systems. The modulation of specific DC subpopulations can have either pro-atherogenic or atheroprotective effects, highlighting the dual pro-inflammatory or tolerogenic roles of DCs. In this work, we provide a comprehensive overview of the evolving roles of DCs and their subtypes in the promotion or limitation of atherosclerosis development. Additionally, we explore antigen pulsing and pharmacological approaches to modulate the function of DCs in the context of atherosclerosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Atherosclerosis 2.0)

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28 pages, 1738 KiB

Open AccessReview

Multi-Modality Imaging of Atheromatous Plaques in Peripheral Arterial Disease: Integrating Molecular and Imaging Markers

by Xiaomeng Wang, Ying-Hwey Nai, Julian Gan, Cheryl Pei Ling Lian, Fraser Kirwan Ryan, Forest Su Lim Tan, Dexter Yak Seng Chan, Jun Jie Ng, Zhiwen Joseph Lo, Tze Tec Chong and Derek John Hausenloy

Int. J. Mol. Sci. 2023, 24(13), 11123; https://doi.org/10.3390/ijms241311123 - 05 Jul 2023

Cited by 1 | Viewed by 2176

Abstract

Peripheral artery disease (PAD) is a common and debilitating condition characterized by the narrowing of the limb arteries, primarily due to atherosclerosis. Non-invasive multi-modality imaging approaches using computed tomography (CT), magnetic resonance imaging (MRI), and nuclear imaging have emerged as valuable tools for assessing PAD atheromatous plaques and vessel walls. This review provides an overview of these different imaging techniques, their advantages, limitations, and recent advancements. In addition, this review highlights the importance of molecular markers, including those related to inflammation, endothelial dysfunction, and oxidative stress, in PAD pathophysiology. The potential of integrating molecular and imaging markers for an improved understanding of PAD is also discussed. Despite the promise of this integrative approach, there remain several challenges, including technical limitations in imaging modalities and the need for novel molecular marker discovery and validation. Addressing these challenges and embracing future directions in the field will be essential for maximizing the potential of molecular and imaging markers for improving PAD patient outcomes. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Atherosclerosis 2.0)

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15 pages, 819 KiB

Open AccessReview

Colchicine in Athero-Thrombosis: Molecular Mechanisms and Clinical Evidence

by Giovanni Cimmino, Francesco S. Loffredo, Gennaro De Rosa and Plinio Cirillo

Int. J. Mol. Sci. 2023, 24(3), 2483; https://doi.org/10.3390/ijms24032483 - 27 Jan 2023

Cited by 5 | Viewed by 3328

Abstract

Several lines of evidence have clearly indicated that inflammation plays a pivotal role in the development of atherosclerosis and of its thrombotic complications such as acute coronary syndromes or ischemic stroke. Thus, it has been postulated that the use of anti-inflammatory agents might be extremely useful to improve cardiovascular outcome. Recently, increasing attention has been reserved to one of the oldest plant-derived drugs still in use in clinical practice, colchicine that has been used as drug to treat inflammatory diseases such gout or Mediterranean fever. To date, current guidelines of the European Society of Cardiology have included colchicine as first line choice for treatment of acute and recurrent pericarditis. Moreover, several studies have investigated its role in the clinical scenarios of cardiovascular disease including chronic and acute coronary syndromes with promising results. In this review, starting from a description of the mechanism(s) involved behind its anti-inflammatory effects, we give an overview on its potential effects in atherothrombosis and finally present an updated overview of clinical evidence on the role of this drug in cardiovascular disease. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Atherosclerosis 2.0)

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