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Cells
Special Issues
Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities
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Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 15508

Special Issue Editors

Dr. Yaw Asare

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Guest Editor
Institute for Stroke and Dementia Research, Klinikum der Universität München, München, Germany
Interests: inflammatory mechanisms in atherosclerosis; innate immune signaling pathways
Dr. Marios Georgakis

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Guest Editor
1. Institute for Stroke and Dementia Research, Klinikum der Universität München, Munich, Germany
2. Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA
3. Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA
Interests: inflammation in atherosclerosis; genetic and clinical epidemiology

Special Issue Information

Dear Colleagues,

Arterial inflammation manifesting as atherosclerosis is the main pathology underlying cardiovascular disease (CVD), including myocardial infarction and ischemic stroke. As a chronic inflammatory disease of the arterial wall, atherosclerosis arises from unbalanced lipid metabolism and maladaptive inflammatory responses. Despite the success of lipid-lowering and anti-hypertensive medications in mitigating complications of atherosclerosis, CVD remains the main cause of death worldwide. Hence, the development of novel preventive and therapeutic strategies is necessary to alleviate the global burden of CVD. Extensive experimental research coupled with epidemiological population-based studies have long suggested a key role of immune mechanisms in atherosclerosis. Only recently, though, did the CANTOS, COLCOT, and LoDoCo2 trials provide proof-of-concept evidence that targeting inflammation can lower CVD risk, thus setting the stage for a new paradigm of atheroprotective treatments. Balanced between atheroprotection and an impaired host response, current research efforts are focused on a better understanding of the immune mechanisms driving atheroprogression and the development of immunotherapies that precisely inhibit atheroprogression. It is therefore the aim of this Special Issue to assemble the current understanding of the cellular and molecular mechanisms involved in the initiation and progression of atherosclerosis, focusing on pathways that can be targeted for vascular protection. Reports from experimental work will be complemented by the results from epidemiological and genetic studies offering a translational bridge to human atherosclerosis.

Dr. Yaw Asare
Dr. Marios Georgakis
Guest Editors

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. Cells 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 2700 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

  • atherosclerosis
  • vascular inflammation
  • monocytes/macrophages
  • endothelial cells
  • IKK/NFκB signaling
  • inflammasome
  • IL-1β
  • cytokines and chemokines
  • neutrophils
  • epigenetic mechanisms
  • Mendelian randomization
  • meta-analyses

Published Papers (6 papers)

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Research

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24 pages, 4584 KiB  
Article
Tissue Inhibitor of Metalloproteinases-1 Interacts with CD74 to Promote AKT Signaling, Monocyte Recruitment Responses, and Vascular Smooth Muscle Cell Proliferation
by Simon Ebert, Lan Zang, Noor Ismail, Michael Otabil, Adrian Fröhlich, Virginia Egea, Susann Ács, Mikkel Hoeberg, Marie-Luise Berres, Christian Weber, José M. A. Moreira, Christian Ries, Jürgen Bernhagen and Omar El Bounkari
Cells 2023, 12(14), 1899; https://doi.org/10.3390/cells12141899 - 20 Jul 2023
Cited by 2 | Viewed by 1842
Abstract
Tissue inhibitor of metalloproteinases-1 (TIMP-1), an important regulator of matrix metalloproteinases (MMPs), has recently been shown to interact with CD74, a receptor for macrophage migration inhibitory factor (MIF). However, the biological effects mediated by TIMP-1 through CD74 remain largely unexplored. Using sequence alignment [...] Read more.
Tissue inhibitor of metalloproteinases-1 (TIMP-1), an important regulator of matrix metalloproteinases (MMPs), has recently been shown to interact with CD74, a receptor for macrophage migration inhibitory factor (MIF). However, the biological effects mediated by TIMP-1 through CD74 remain largely unexplored. Using sequence alignment and in silico protein–protein docking analysis, we demonstrated that TIMP-1 shares residues with both MIF and MIF-2, crucial for CD74 binding, but not for CXCR4. Subcellular colocalization, immunoprecipitation, and internalization experiments supported these findings, demonstrating that TIMP-1 interacts with surface-expressed CD74, resulting in its internalization in a dose-dependent manner, as well as with a soluble CD74 ectodomain fragment (sCD74). This prompted us to study the effects of the TIMP-1–CD74 axis on monocytes and vascular smooth muscle cells (VSCMs) to assess its impact on vascular inflammation. A phospho-kinase array revealed the activation of serine/threonine kinases by TIMP-1 in THP-1 pre-monocytes, in particular AKT. Similarly, TIMP-1 dose-dependently triggered the phosphorylation of AKT and ERK1/2 in primary human monocytes. Importantly, Transwell migration, 3D-based Chemotaxis, and flow adhesion assays demonstrated that TIMP-1 engagement of CD74 strongly promotes the recruitment response of primary human monocytes, while live cell imaging studies revealed a profound activating effect on VSMC proliferation. Finally, re-analysis of scRNA-seq data highlighted the expression patterns of TIMP-1 and CD74 in human atherosclerotic lesions, thus, together with our experimental data, indicating a role for the TIMP-1–CD74 axis in vascular inflammation and atherosclerosis. Full article
(This article belongs to the Special Issue Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities)
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Review

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22 pages, 1652 KiB  
Review
Innate Immune Pathways in Atherosclerosis—From Signaling to Long-Term Epigenetic Reprogramming
by Arailym Aronova, Federica Tosato, Nawraa Naser and Yaw Asare
Cells 2023, 12(19), 2359; https://doi.org/10.3390/cells12192359 - 26 Sep 2023
Viewed by 1868
Abstract
Innate immune pathways play a crucial role in the development of atherosclerosis, from sensing initial danger signals to the long-term reprogramming of immune cells. Despite the success of lipid-lowering therapy, anti-hypertensive medications, and other measures in reducing complications associated with atherosclerosis, cardiovascular disease [...] Read more.
Innate immune pathways play a crucial role in the development of atherosclerosis, from sensing initial danger signals to the long-term reprogramming of immune cells. Despite the success of lipid-lowering therapy, anti-hypertensive medications, and other measures in reducing complications associated with atherosclerosis, cardiovascular disease (CVD) remains the leading cause of death worldwide. Consequently, there is an urgent need to devise novel preventive and therapeutic strategies to alleviate the global burden of CVD. Extensive experimental research and epidemiological studies have demonstrated the dominant role of innate immune mechanisms in the progression of atherosclerosis. Recently, landmark trials including CANTOS, COLCOT, and LoDoCo2 have provided solid evidence demonstrating that targeting innate immune pathways can effectively reduce the risk of CVD. These groundbreaking trials mark a significant paradigm shift in the field and open new avenues for atheroprotective treatments. It is therefore crucial to comprehend the intricate interplay between innate immune pathways and atherosclerosis for the development of targeted therapeutic interventions. Additionally, unraveling the mechanisms underlying long-term reprogramming may offer novel strategies to reverse the pro-inflammatory phenotype of immune cells and restore immune homeostasis in atherosclerosis. In this review, we present an overview of the innate immune pathways implicated in atherosclerosis, with a specific focus on the signaling pathways driving chronic inflammation in atherosclerosis and the long-term reprogramming of immune cells within atherosclerotic plaque. Elucidating the molecular mechanisms governing these processes presents exciting opportunities for the development of a new class of immunotherapeutic approaches aimed at reducing inflammation and promoting plaque stability. By addressing these aspects, we can potentially revolutionize the management of atherosclerosis and its associated cardiovascular complications. Full article
(This article belongs to the Special Issue Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities)
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17 pages, 886 KiB  
Review
T Cells in Atherosclerosis: Key Players in the Pathogenesis of Vascular Disease
by Hannah Hinkley, Daniel A. Counts, Elizabeth VonCanon and Michael Lacy
Cells 2023, 12(17), 2152; https://doi.org/10.3390/cells12172152 - 26 Aug 2023
Cited by 7 | Viewed by 2457
Abstract
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-rich plaques within arterial walls. T cells play a pivotal role in the pathogenesis of atherosclerosis in which they help orchestrate immune responses and contribute to plaque development and instability. Here, we [...] Read more.
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-rich plaques within arterial walls. T cells play a pivotal role in the pathogenesis of atherosclerosis in which they help orchestrate immune responses and contribute to plaque development and instability. Here, we discuss the recognition of atherosclerosis-related antigens that may trigger T cell activation together with additional signaling from co-stimulatory molecules and lesional cytokines. Although few studies have indicated candidates for the antigen specificity of T cells in atherosclerosis, further research is needed. Furthermore, we describe the pro-atherogenic and atheroprotective roles of diverse subsets of T cells such as CD4+ helper, CD8+ cytotoxic, invariant natural killer, and γδ T cells. To classify and quantify T cell subsets in atherosclerosis, we summarize current methods to analyze cellular heterogeneity including single cell RNA sequencing and T cell receptor (TCR) sequencing. Further insights into T cell biology will help shed light on the immunopathology of atherosclerosis, inform potential therapeutic interventions, and pave the way for precision medicine approaches in combating cardiovascular disease. Full article
(This article belongs to the Special Issue Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities)
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20 pages, 6512 KiB  
Review
Imaging Carotid Plaque Inflammation Using Positron Emission Tomography: Emerging Role in Clinical Stroke Care, Research Applications, and Future Directions
by John J. McCabe, Nicholas R. Evans, Sarah Gorey, Shiv Bhakta, James H. F. Rudd and Peter J. Kelly
Cells 2023, 12(16), 2073; https://doi.org/10.3390/cells12162073 - 15 Aug 2023
Cited by 1 | Viewed by 1653
Abstract
Atherosclerosis is a chronic systemic inflammatory condition of the vasculature and a leading cause of stroke. Luminal stenosis severity is an important factor in determining vascular risk. Conventional imaging modalities, such as angiography or duplex ultrasonography, are used to quantify stenosis severity and [...] Read more.
Atherosclerosis is a chronic systemic inflammatory condition of the vasculature and a leading cause of stroke. Luminal stenosis severity is an important factor in determining vascular risk. Conventional imaging modalities, such as angiography or duplex ultrasonography, are used to quantify stenosis severity and inform clinical care but provide limited information on plaque biology. Inflammatory processes are central to atherosclerotic plaque progression and destabilization. 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) is a validated technique for quantifying plaque inflammation. In this review, we discuss the evolution of FDG-PET as an imaging modality to quantify plaque vulnerability, challenges in standardization of image acquisition and analysis, its potential application to routine clinical care after stroke, and the possible role it will play in future drug discovery. Full article
(This article belongs to the Special Issue Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities)
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13 pages, 928 KiB  
Review
The Role of Macrophages in the Pathogenesis of Atherosclerosis
by Alexander V. Blagov, Alexander M. Markin, Anastasia I. Bogatyreva, Taisiya V. Tolstik, Vasily N. Sukhorukov and Alexander N. Orekhov
Cells 2023, 12(4), 522; https://doi.org/10.3390/cells12040522 - 5 Feb 2023
Cited by 27 | Viewed by 4924
Abstract
A wide variety of cell populations, including both immune and endothelial cells, participate in the pathogenesis of atherosclerosis. Among these groups, macrophages deserve special attention because different populations of them can have completely different effects on atherogenesis and inflammation in atherosclerosis. In the [...] Read more.
A wide variety of cell populations, including both immune and endothelial cells, participate in the pathogenesis of atherosclerosis. Among these groups, macrophages deserve special attention because different populations of them can have completely different effects on atherogenesis and inflammation in atherosclerosis. In the current review, the significance of different phenotypes of macrophages in the progression or regression of atherosclerosis will be considered, including their ability to become the foam cells and the consequences of this event, as well as their ability to create a pro-inflammatory or anti-inflammatory medium at the site of atherosclerotic lesions as a result of cytokine production. In addition, several therapeutic strategies directed to the modulation of macrophage activity, which can serve as useful ideas for future drug developments, will be considered. Full article
(This article belongs to the Special Issue Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities)
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Other

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10 pages, 979 KiB  
Perspective
The Impact of the Nervous System on Arteries and the Heart: The Neuroimmune Cardiovascular Circuit Hypothesis
by Sarajo K. Mohanta, Ting Sun, Shu Lu, Zhihua Wang, Xi Zhang, Changjun Yin, Christian Weber and Andreas J. R. Habenicht
Cells 2023, 12(20), 2485; https://doi.org/10.3390/cells12202485 - 19 Oct 2023
Cited by 1 | Viewed by 1824
Abstract
Three systemic biological systems, i.e., the nervous, the immune, and the cardiovascular systems, form a mutually responsive and forward-acting tissue network to regulate acute and chronic cardiovascular function in health and disease. Two sub-circuits within the cardiovascular system have been described, the artery [...] Read more.
Three systemic biological systems, i.e., the nervous, the immune, and the cardiovascular systems, form a mutually responsive and forward-acting tissue network to regulate acute and chronic cardiovascular function in health and disease. Two sub-circuits within the cardiovascular system have been described, the artery brain circuit (ABC) and the heart brain circuit (HBC), forming a large cardiovascular brain circuit (CBC). Likewise, the nervous system consists of the peripheral nervous system and the central nervous system with their functional distinct sensory and effector arms. Moreover, the immune system with its constituents, i.e., the innate and the adaptive immune systems, interact with the CBC and the nervous system at multiple levels. As understanding the structure and inner workings of the CBC gains momentum, it becomes evident that further research into the CBC may lead to unprecedented classes of therapies to treat cardiovascular diseases as multiple new biologically active molecules are being discovered that likely affect cardiovascular disease progression. Here, we weigh the merits of integrating these recent observations in cardiovascular neurobiology into previous views of cardiovascular disease pathogeneses. These considerations lead us to propose the Neuroimmune Cardiovascular Circuit Hypothesis. Full article
(This article belongs to the Special Issue Vascular Inflammation and Atherosclerosis: From Basic Mechanisms to Therapeutic Opportunities)
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