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The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis
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The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 October 2023) | Viewed by 11312

Special Issue Editor

Dr. Josip Andelo Borovac

E-Mail Website
Guest Editor
Cardiovascular Diseases Department, University Hospital of Split, 21000 Split, Croatia
Interests: interventional cardiology; heart failure; acute coronary syndrome; myocardial infarction; thrombosis; percutaneous coronary intervention; atherosclerosis; clinical trials
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Atherosclerosis is the leading pathogenetic cause of cardiovascular disease (CVD), being of great public health relevance due to the high associated rates of morbidity, mortality, and healthcare expenditures in modern-day societies. The pathophysiology of atherosclerosis is multifaceted and when this inherent biological process progresses significantly within the vessel it can clinically manifest as myocardial infarction, stroke, peripheral artery disease, and even renal failure. These complications are often severe for the individual and can result in death or permanent disability. Although substantial advances have been made in treating atherosclerosis and its complications in recent decades, a vast array of molecular mechanisms and therapeutic targets involved in atherogenesis have yet to be unraveled. For these reasons, research efforts that will identify the novel therapeutic targets and molecular mechanisms that are operative in atherosclerosis are of exceptional importance. Only such research efforts will allow the development of effective treatment modalities and precise individually tailored therapies with the potential to prevent or mitigate CVD.

This Special Issue of the International Journal of Molecular Sciences welcomes all original articles as well as state-of-the-art reviews with a strong emphasis on molecular biology and molecular medicine, focused on atherosclerosis and its complications. This includes, but is not limited to, pathophysiological mechanisms that are deeply crosslinked in atherosclerosis such as systemic and local inflammation, adaptive and innate immune system responses, vascular endothelial injury, lipid accumulation, aberrant vascular smooth muscle cell development and calcification, and others. Similarly, works focused on mechanisms and therapeutic efforts involving neoatherosclerosis and neointimal hyperplasia, as well as translational cardiology submissions, are welcome. Equally so, submissions focused on translational or clinical aspects of novel molecular biomarkers used for the diagnosis and prognosis of atherosclerotic heart disease are highly sought. Finally, molecular-level research identifying novel molecules as potential targets in atherosclerosis is welcome.

Dr. Josip Andelo Borovac
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

  • atherosclerosis
  • biomarkers
  • endothelial dysfunction
  • immunological response
  • inflammation
  • lipid metabolism
  • neoatherosclerosis
  • oxidative stress
  • vascular calcification
  • vascular smooth muscle cells

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 235 KiB  
Editorial
The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis: From Basic Research to Interventional Cardiology
by Josip Andelo Borovac
Int. J. Mol. Sci. 2024, 25(9), 4936; https://doi.org/10.3390/ijms25094936 - 30 Apr 2024
Viewed by 312
Abstract
The goal of this Special Issue was to collect original pieces as well as state-of-the-art review articles from scientists and research groups with specific interests in atherosclerosis research [...] Full article
(This article belongs to the Special Issue The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis)

Research

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9 pages, 1610 KiB  
Article
Circulating Soluble TREM2 and Cardiovascular Outcome in Cohort Study of Coronary Atherosclerosis Patients
by Valeri Cuciuc, Sagi Tshori, Livi Grib, Gal Sella, Ortal Tuvali, Igor Volodarsky, Michael Welt, Michael Fassler, Sara Shimoni and Jacob George
Int. J. Mol. Sci. 2022, 23(21), 13121; https://doi.org/10.3390/ijms232113121 - 28 Oct 2022
Cited by 3 | Viewed by 1486
Abstract
Triggering Receptor Expressed in Myeloid Cells 2 (TREM2) is a membrane receptor in myeloid cells that mediates cellular phagocytosis and inflammation. TREM2 and its soluble extracellular domain are clearly implicated in neuroinflammation and neurodegeneration. sTREM2 is also expressed in atherosclerotic macrophages. We hypothesized [...] Read more.
Triggering Receptor Expressed in Myeloid Cells 2 (TREM2) is a membrane receptor in myeloid cells that mediates cellular phagocytosis and inflammation. TREM2 and its soluble extracellular domain are clearly implicated in neuroinflammation and neurodegeneration. sTREM2 is also expressed in atherosclerotic macrophages. We hypothesized that sTREM2 would predict cardiovascular mortality in patients with established coronary atherosclerosis (CAD). Consecutive patients undergoing coronary angiography with the establishment of the diagnosis of CAD (n = 230) and without CAD (n = 53) were tested for their baseline serum sTREM2 levels. All patients were followed up for 84 months or until death occurred. sTREM2 correlated with age; however, no association was found between sTREM2 and the number of atherosclerotic vessels involved (p = 0.642). After 84 months of follow-up, 68 out of the 230 CAD patients had died. After adjusting for age and other risk factors, the adjusted hazard ratio for the highest quartile of sTREM2 was 2.37 (95% confidence interval 1.17–4.83) for death. In patients with established CAD, serum sTREM2 appears to predict cardiovascular death as a potential surrogate for plaque rupture. TREM2 and its soluble extracellular form might be implicated in the fate of the atherosclerotic plaque, but corroboration within larger studies is needed. Full article
(This article belongs to the Special Issue The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis)
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Review

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24 pages, 2025 KiB  
Review
Novel Insights into the Molecular Mechanisms of Atherosclerosis
by Armanda Wojtasińska, Weronika Frąk, Wiktoria Lisińska, Natalia Sapeda, Ewelina Młynarska, Jacek Rysz and Beata Franczyk
Int. J. Mol. Sci. 2023, 24(17), 13434; https://doi.org/10.3390/ijms241713434 - 30 Aug 2023
Cited by 15 | Viewed by 2567
Abstract
Atherosclerosis is one of the most fatal diseases in the world. The associated thickening of the arterial wall and its background and consequences make it a very composite disease entity with many mechanisms that lead to its creation. It is an active process, [...] Read more.
Atherosclerosis is one of the most fatal diseases in the world. The associated thickening of the arterial wall and its background and consequences make it a very composite disease entity with many mechanisms that lead to its creation. It is an active process, and scientists from various branches are engaged in research, including molecular biologists, cardiologists, and immunologists. This review summarizes the available information on the pathophysiological implications of atherosclerosis, focusing on endothelium dysfunction, inflammatory factors, aging, and uric acid, vitamin D, and miRNA expression as recent evidence of interactions of the molecular and cellular elements. Analyzing new discoveries for the underlying causes of this condition assists the general research to improve understanding of the mechanism of pathophysiology and thus prevention of cardiovascular diseases. Full article
(This article belongs to the Special Issue The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis)
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21 pages, 1589 KiB  
Review
Coronary “Microvascular Dysfunction”: Evolving Understanding of Pathophysiology, Clinical Implications, and Potential Therapeutics
by Chun Yeung Kei, Kuljit Singh, Rustem F. Dautov, Thanh H. Nguyen, Yuliy Y. Chirkov and John D. Horowitz
Int. J. Mol. Sci. 2023, 24(14), 11287; https://doi.org/10.3390/ijms241411287 - 10 Jul 2023
Cited by 6 | Viewed by 2109
Abstract
Until recently, it has been generally held that stable angina pectoris (SAP) primarily reflects the presence of epicardial coronary artery stenoses due to atheromatous plaque(s), while acute myocardial infarction (AMI) results from thrombus formation on ruptured plaques. This concept is now challenged, especially [...] Read more.
Until recently, it has been generally held that stable angina pectoris (SAP) primarily reflects the presence of epicardial coronary artery stenoses due to atheromatous plaque(s), while acute myocardial infarction (AMI) results from thrombus formation on ruptured plaques. This concept is now challenged, especially by results of the ORBITA and ISCHEMIA trials, which showed that angioplasty/stenting does not substantially relieve SAP symptoms or prevent AMI or death in such patients. These disappointing outcomes serve to redirect attention towards anomalies of small coronary physiology. Recent studies suggest that coronary microvasculature is often both structurally and physiologically abnormal irrespective of the presence or absence of large coronary artery stenoses. Structural remodelling of the coronary microvasculature appears to be induced primarily by inflammation initiated by mast cell, platelet, and neutrophil activation, leading to erosion of the endothelial glycocalyx. This leads to the disruption of laminar flow and the facilitation of endothelial platelet interaction. Glycocalyx shedding has been implicated in the pathophysiology of coronary artery spasm, cardiovascular ageing, AMI, and viral vasculitis. Physiological dysfunction is closely linked to structural remodelling and occurs in most patients with myocardial ischemia, irrespective of the presence or absence of large-vessel stenoses. Dysfunction includes the impairment of platelet and vascular responsiveness to autocidal coronary vasodilators, such as nitric oxide, prostacyclin, and hydrogen sulphide, and predisposes both to coronary vasoconstriction and to a propensity for microthrombus formation. These findings emphasise the need for new directions in medical therapeutics for patients with SAP, as well as a wide range of other cardiovascular disorders. Full article
(This article belongs to the Special Issue The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis)
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16 pages, 850 KiB  
Review
Emerging Therapies for the Treatment of Atherosclerotic Cardiovascular Disease: From Bench to Bedside
by Marko Kumric, Hrvoje Urlic, Josko Bozic, Marino Vilovic, Tina Ticinovic Kurir, Duska Glavas, Dino Miric, Jaksa Zanchi, Anteo Bradaric-Slujo, Mislav Lozo and Josip A. Borovac
Int. J. Mol. Sci. 2023, 24(9), 8062; https://doi.org/10.3390/ijms24098062 - 29 Apr 2023
Cited by 2 | Viewed by 2326
Abstract
Primarily a consequence of sedentary lifestyle, atherosclerosis has already reached pandemic proportions, and with every year the burden of it is only increasing. As low-density lipoprotein cholesterol (LDL-C) represents a crucial factor in atherosclerosis formation and progression, stringent lipid-lowering therapy could conceivably be [...] Read more.
Primarily a consequence of sedentary lifestyle, atherosclerosis has already reached pandemic proportions, and with every year the burden of it is only increasing. As low-density lipoprotein cholesterol (LDL-C) represents a crucial factor in atherosclerosis formation and progression, stringent lipid-lowering therapy could conceivably be the key to preventing the unfavorable outcomes that arise as a consequence of atherosclerosis. The use of statins in lipid-lowering is often burdened by adverse events or is insufficient to prevent cardiovascular events as a monotherapy. Therefore, in the present review, the authors aimed to discuss the underlying mechanisms of dyslipidemia and associated atherosclerotic cardiovascular disease (ASCVD) and preclinical and clinical trials of novel therapeutic approaches to its treatment, some of which are still in the early stages of development. Apart from novel therapies, a novel change in perspective is needed. Specifically, the critical objective in the future management of ASCVD is to embrace emerging evidence in the field of atherosclerosis, because clinicians are often burden by common practice and personal experience, both of which have so far been shown to be futile in the setting of atherosclerosis. Full article
(This article belongs to the Special Issue The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis)
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23 pages, 6125 KiB  
Review
Intracoronary Imaging of Coronary Atherosclerotic Plaque: From Assessment of Pathophysiological Mechanisms to Therapeutic Implication
by Filippo Luca Gurgoglione, Andrea Denegri, Michele Russo, Camilla Calvieri, Giorgio Benatti and Giampaolo Niccoli
Int. J. Mol. Sci. 2023, 24(6), 5155; https://doi.org/10.3390/ijms24065155 - 08 Mar 2023
Cited by 5 | Viewed by 1880
Abstract
Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality worldwide. Several cardiovascular risk factors are implicated in atherosclerotic plaque promotion and progression and are responsible for the clinical manifestations of coronary artery disease (CAD), ranging from chronic to acute coronary syndromes [...] Read more.
Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality worldwide. Several cardiovascular risk factors are implicated in atherosclerotic plaque promotion and progression and are responsible for the clinical manifestations of coronary artery disease (CAD), ranging from chronic to acute coronary syndromes and sudden coronary death. The advent of intravascular imaging (IVI), including intravascular ultrasound, optical coherence tomography and near-infrared diffuse reflectance spectroscopy has significantly improved the comprehension of CAD pathophysiology and has strengthened the prognostic relevance of coronary plaque morphology assessment. Indeed, several atherosclerotic plaque phenotype and mechanisms of plaque destabilization have been recognized with different natural history and prognosis. Finally, IVI demonstrated benefits of secondary prevention therapies, such as lipid-lowering and anti-inflammatory agents. The purpose of this review is to shed light on the principles and properties of available IVI modalities along with their prognostic significance. Full article
(This article belongs to the Special Issue The Molecular Mechanisms and Therapeutic Targets of Atherosclerosis)
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