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Atherosclerosis: From Molecular Biology to Therapeutic Perspective: 6th Edition
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Atherosclerosis: From Molecular Biology to Therapeutic Perspective: 6th Edition

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: 20 May 2025 | Viewed by 7770

Special Issue Editor

Dr. Ida Daniela Perrotta

E-Mail Website
Guest Editor
Department of Biology, Ecology and Earth Sciences, Centre for Microscopy and Microanalysis (CM2), University of Calabria, Arcavacata di Rende, 87036 Cosenza, Italy
Interests: atherosclerosis; vascular smooth muscle cell; inflammation; endothelium; cell senescence; apoptosis; lipid metabolism; oxidative stress; nitric oxide; exosomes; vascular calcification; cytokines; growth factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although studies on the molecular biology of atherogenesis have become the focus of modern atherosclerosis research, the multifactorial pathogenesis of the disease has not been fully elucidated to date. Atherosclerosis is a fibroproliferative disease that proceeds through a series of pathological events involving the inflammatory and immune systems as well as the different types of cells and matrix proteins of the vascular wall. The disease is accompanied by the subendothelial accumulation of lipids and fibrous connective tissue, the phenotypic modulation of SMCs, and the migration of a group of cells, notably monocytes and T cells, through the vascular endothelium in response to inflammation. Along with the traditional cardiovascular risk factors, many other molecular determinants have a role in the appearance, progression, and complication of the disease. Inflammatory cytokines, growth factors, markers of oxidative stress, cell death signals, and mediators of vascular tone all participate in the inflammatory response of atherosclerosis via multiple intricate pathways. Also, arterial wall calcification is considered a direct marker of atherosclerotic disease, yet its underlying molecular mechanisms remain to be elucidated. Other important contributors to atherosclerosis are the exosomes and their miRNAs whose role and interactions with the microenvironment of the plaque can be exploited therapeutically.

This Special Issue on “Atherosclerosis: From Molecular Biology to Therapeutic Perspective 6.0” welcomes original research articles and reviews in the field, with a focus on (but not limited to) the molecular mechanisms mediating vascular inflammation, endothelial dysfunction, SMC biology, immune-metabolic interactions, apoptosis, cell-to-cell communication, lipid metabolism, and vascular cell senescence.

Dr. Ida Daniela Perrotta
Guest Editor

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Keywords

  • atherosclerosis
  • vascular smooth muscle cell
  • inflammation
  • endothelium
  • cell senescence
  • apoptosis
  • lipid metabolism
  • oxidative stress
  • nitric oxide
  • exosomes
  • vascular calcification
  • cytokines
  • growth factors

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Published Papers (4 papers)

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Research

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14 pages, 2215 KiB  
Article
Influence of Atherosclerosis-Associated Risk Factors on Expression of Endothelin Receptors in Advanced Atherosclerosis
by Oliver Herbers, Carsten Höltke, Marco Virgilio Usai, Jana Hochhalter, Moushami Mallik, Moritz Wildgruber, Anne Helfen and Miriam Stölting
Int. J. Mol. Sci. 2025, 26(5), 2310; https://doi.org/10.3390/ijms26052310 - 5 Mar 2025
Viewed by 491
Abstract
Endothelin-1 (ET-1) levels are altered in atherosclerosis, while the roles of the endothelin receptors ETAR and ETBR during the pathogenesis of atherosclerosis remain unclear. Therefore, the focus of this study was to clarify how endothelin receptors are expressed in [...] Read more.
Endothelin-1 (ET-1) levels are altered in atherosclerosis, while the roles of the endothelin receptors ETAR and ETBR during the pathogenesis of atherosclerosis remain unclear. Therefore, the focus of this study was to clarify how endothelin receptors are expressed in advanced human atherosclerotic plaques and how this is related to atherosclerotic risk factors. Ex vivo expression analysis was performed by quantitative real-time PCR (qRT-PCR) of 98 atherosclerotic plaques and controls that were obtained from adult patients undergoing vascular surgery. Correlation analyses of atherosclerosis-promoting factors were accomplished using a linear regression model. We found an overall reduced expression of ET receptors and smooth muscle actin (SMA), a marker of healthy vascular smooth muscle cells, in atherosclerotic plaques, whereas the levels of ET-1 and matrix metalloproteinase 2 (MMP-2), a marker of atherosclerosis progression, remained unchanged. Reduced expression was predominantly correlated with hypertension, which affects both receptors as well as SMA. Age, body mass index (BMI) and gender also correlated with either ETAR, ETBR or SMA expression in advanced plaques. In contrast, no effect of diabetes mellitus or smoking was found, indicating an ancillary effect of those risk factors. The results of our study indicate that endothelin receptor expression during the pathogenesis of atherosclerosis is predominantly correlated with hypertension. Full article
(This article belongs to the Special Issue Atherosclerosis: From Molecular Biology to Therapeutic Perspective: 6th Edition)
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13 pages, 2682 KiB  
Article
Glucose-Dependent Insulinotropic Polypeptide Inhibits AGE-Induced NADPH Oxidase-Derived Oxidative Stress Generation and Foam Cell Formation in Macrophages Partly via AMPK Activation
by Michishige Terasaki, Hironori Yashima, Yusaku Mori, Tomomi Saito, Naoto Inoue, Takanori Matsui, Naoya Osaka, Tomoki Fujikawa, Makoto Ohara and Sho-ichi Yamagishi
Int. J. Mol. Sci. 2024, 25(17), 9724; https://doi.org/10.3390/ijms25179724 - 8 Sep 2024
Cited by 2 | Viewed by 1605
Abstract
Glucose-dependent insulinotropic polypeptide (GIP) of the incretin group has been shown to exert pleiotropic actions. There is growing evidence that advanced glycation end products (AGEs), senescent macromolecules formed at an accelerated rate under chronic hyperglycemic conditions, play a role in the pathogenesis of [...] Read more.
Glucose-dependent insulinotropic polypeptide (GIP) of the incretin group has been shown to exert pleiotropic actions. There is growing evidence that advanced glycation end products (AGEs), senescent macromolecules formed at an accelerated rate under chronic hyperglycemic conditions, play a role in the pathogenesis of atherosclerotic cardiovascular disease in diabetes. However, whether and how GIP could inhibit the AGE-induced foam cell formation of macrophages, an initial step of atherosclerosis remains to be elucidated. In this study, we address these issues. We found that AGEs increased oxidized low-density-lipoprotein uptake into reactive oxygen species (ROS) generation and Cdk5 and CD36 gene expressions in human U937 macrophages, all of which were significantly blocked by [D-Ala2]GIP(1–42) or an inhibitor of NADPH oxidase activity. An inhibitor of AMP-activated protein kinase (AMPK) attenuated all of the beneficial effects of [D-Ala2]GIP(1–42) on AGE-exposed U937 macrophages, whereas an activator of AMPK mimicked the effects of [D-Ala2]GIP(1–42) on foam cell formation, ROS generation, and Cdk5 and CD36 gene expressions in macrophages. The present study suggests that [D-Ala2]GIP(1–42) could inhibit the AGE-RAGE-induced, NADPH oxidase-derived oxidative stress generation in U937 macrophages via AMPK activation and subsequently suppress macrophage foam cell formation by reducing the Cdk5-CD36 pathway. Full article
(This article belongs to the Special Issue Atherosclerosis: From Molecular Biology to Therapeutic Perspective: 6th Edition)
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Review

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32 pages, 1002 KiB  
Review
Atherosclerosis and the Bidirectional Relationship Between Cancer and Cardiovascular Disease: From Bench to Bedside, Part 2 Management
by Giuseppina Gallucci, Mario Larocca, Alessandro Navazio, Fabio Maria Turazza, Alessandro Inno, Maria Laura Canale, Stefano Oliva, Giulia Besutti, Andrea Tedeschi, Daniela Aschieri, Antonio Russo, Stefania Gori, Nicola Silvestris, Carmine Pinto and Luigi Tarantini
Int. J. Mol. Sci. 2025, 26(1), 334; https://doi.org/10.3390/ijms26010334 - 2 Jan 2025
Cited by 1 | Viewed by 1417
Abstract
The first part of this review highlighted the evolving landscape of atherosclerosis, noting emerging cardiometabolic risk factors, the growing impact of exposomes, and social determinants of health. The prominent role of atherosclerosis in the bidirectional relationship between cardiovascular disease and cancer was also [...] Read more.
The first part of this review highlighted the evolving landscape of atherosclerosis, noting emerging cardiometabolic risk factors, the growing impact of exposomes, and social determinants of health. The prominent role of atherosclerosis in the bidirectional relationship between cardiovascular disease and cancer was also discussed. In this second part, we examine the complex interplay between multimorbid cardio-oncologic patients, cardiometabolic risk factors, and the harmful environments that lend a “syndemic” nature to these chronic diseases. We summarize management strategies targeting disordered cardiometabolic factors to mitigate cardiovascular disease and explore molecular mechanisms enabling more tailored therapies. Importantly, we emphasize the early interception of atherosclerosis through multifactorial interventions that detect subclinical signs (via biomarkers and imaging) to treat modifiable risk factors and prevent clinical events. A concerted preventive effort—referred to by some as a “preventome”—is essential to reduce the burden of atherosclerosis-driven chronic diseases, shifting from mere chronic disease management to the proactive promotion of “chronic health”. Full article
(This article belongs to the Special Issue Atherosclerosis: From Molecular Biology to Therapeutic Perspective: 6th Edition)
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22 pages, 6116 KiB  
Review
The Implications of Aging on Vascular Health
by Bulbul Ahmed, Ahmed A. Rahman, Sujin Lee and Rajeev Malhotra
Int. J. Mol. Sci. 2024, 25(20), 11188; https://doi.org/10.3390/ijms252011188 - 17 Oct 2024
Cited by 6 | Viewed by 3916
Abstract
Vascular aging encompasses structural and functional changes in the vasculature, significantly contributing to cardiovascular diseases, which are the leading cause of death globally. The incidence and prevalence of these diseases increase with age, with most morbidity and mortality attributed to myocardial infarction and [...] Read more.
Vascular aging encompasses structural and functional changes in the vasculature, significantly contributing to cardiovascular diseases, which are the leading cause of death globally. The incidence and prevalence of these diseases increase with age, with most morbidity and mortality attributed to myocardial infarction and stroke. Diagnosing and intervening in vascular aging while understanding the mechanisms behind age-induced vascular phenotypic and pathophysiological alterations offers the potential for delaying and preventing cardiovascular mortality in an aging population. This review delves into various aspects of vascular aging by examining age-related changes in arterial health at the cellular level, including endothelial dysfunction, cellular senescence, and vascular smooth muscle cell transdifferentiation, as well as at the structural level, including arterial stiffness and changes in wall thickness and diameter. We also explore aging-related changes in perivascular adipose tissue deposition, arterial collateralization, and calcification, providing insights into the physiological and pathological implications. Overall, aging induces phenotypic changes that augment the vascular system’s susceptibility to disease, even in the absence of traditional risk factors, such as hypertension, diabetes, obesity, and smoking. Overall, age-related modifications in cellular phenotype and molecular homeostasis increase the vulnerability of the arterial vasculature to structural and functional alterations, thereby accelerating cardiovascular risk. Increasing our understanding of these modifications is crucial for success in delaying or preventing cardiovascular diseases. Non-invasive techniques, such as measuring carotid intima-media thickness, pulse wave velocity, and flow-mediated dilation, as well as detecting vascular calcifications, can be used for the early detection of vascular aging. Targeting specific pathological mechanisms, such as cellular senescence and enhancing angiogenesis, holds promise for innovative therapeutic approaches. Full article
(This article belongs to the Special Issue Atherosclerosis: From Molecular Biology to Therapeutic Perspective: 6th Edition)
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