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Cells
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Cellular and Molecular Mechanisms Underlying Large-Vessel Vasculitis
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Cellular and Molecular Mechanisms Underlying Large-Vessel Vasculitis

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 4491

Special Issue Editors

Dr. Martina Bonacini

E-Mail Website
Guest Editor
Clinical Immunology, Allergy and Advanced Biotechnologies Unit, Azienda USL-IRCCS di Reggio Emilia, 42123 Reggio Emilia, Italy
Interests: autoimmune disorders; inflammation; cytokines; intracellular signaling; molecular biology
Dr. Francesco Muratore

E-Mail Website
Guest Editor
1. Rheumatology Unit, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy
2. Department of Surgery, University of Modena and Reggio Emilia, Modena, Italy
Interests: vasculitis; giant cell arteritis; Takayasu arteritis; imaging; treatment

Special Issue Information

Dear Colleagues,

Large-Vessel Vasculitis manifestations include Giant-Cell Arteritis and Takayasu’s Arteritis. In addition, patients with Behçet’s Disease may experience involvement of large-size vessels. Despite the progress in recent years in the field of Large-Vessel Vasculitis, there are several unmet needs regarding the pathogenesis, diagnosis, and the definition of disease activity. Moreover, the identification of new therapeutic approaches for refractory/relapsing patients is essential. Finally, the shortage of cellular and animal models of Large-Vessel Vasculitis makes the conduction of pathogenesis studies difficult.

Increasing the knowledge of cellular and molecular mechanisms of these diseases can top up these gaps of knowledge and get better the patients’ management.

This Special Issue is focused on the identification of new mechanisms underlying Large-Vessel Vasculitis as well as on the new therapeutic approaches.    

Dr. Martina Bonacini
Dr. Francesco Muratore
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

  • large-vessel vasculitis
  • giant cell arteritis
  • Takayasu’s arteritis
  • Behcet’s Disease
  • in vitro/animal models
  • novel therapy

Published Papers (3 papers)

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Review

31 pages, 2454 KiB  
Review
Current Insights into Tissue Injury of Giant Cell Arteritis: From Acute Inflammatory Responses towards Inappropriate Tissue Remodeling
by Dimitris Anastasios Palamidas, Loukas Chatzis, Maria Papadaki, Ilias Gissis, Konstantinos Kambas, Evangelos Andreakos, Andreas V. Goules and Athanasios G. Tzioufas
Cells 2024, 13(5), 430; https://doi.org/10.3390/cells13050430 - 29 Feb 2024
Viewed by 1381
Abstract
Giant cell arteritis (GCA) is an autoimmune disease affecting large vessels in patients over 50 years old. It is an exemplary model of a classic inflammatory disorder with IL-6 playing the leading role. The main comorbidities that may appear acutely or chronically are [...] Read more.
Giant cell arteritis (GCA) is an autoimmune disease affecting large vessels in patients over 50 years old. It is an exemplary model of a classic inflammatory disorder with IL-6 playing the leading role. The main comorbidities that may appear acutely or chronically are vascular occlusion leading to blindness and thoracic aorta aneurysm formation, respectively. The tissue inflammatory bulk is expressed as acute or chronic delayed-type hypersensitivity reactions, the latter being apparent by giant cell formation. The activated monocytes/macrophages are associated with pronounced Th1 and Th17 responses. B-cells and neutrophils also participate in the inflammatory lesion. However, the exact order of appearance and mechanistic interactions between cells are hindered by the lack of cellular and molecular information from early disease stages and accurate experimental models. Recently, senescent cells and neutrophil extracellular traps have been described in tissue lesions. These structures can remain in tissues for a prolonged period, potentially favoring inflammatory responses and tissue remodeling. In this review, current advances in GCA pathogenesis are discussed in different inflammatory phases. Through the description of these—often overlapping—phases, cells, molecules, and small lipid mediators with pathogenetic potential are described. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms Underlying Large-Vessel Vasculitis)
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17 pages, 1097 KiB  
Review
The Contribution of Innate Immunity in Large-Vessel Vasculitis: Detangling New Pathomechanisms beyond the Onset of Vascular Inflammation
by Lidia La Barbera, Chiara Rizzo, Federica Camarda, Giuseppe Miceli, Antonino Tuttolomondo and Giuliana Guggino
Cells 2024, 13(3), 271; https://doi.org/10.3390/cells13030271 - 1 Feb 2024
Cited by 1 | Viewed by 1217
Abstract
Large-vessel vasculitis (LVV) are autoimmune and autoinflammatory diseases focused on vascular inflammation. The central core of the intricate immunological and molecular network resides in the disruption of the “privileged immune state” of the arterial wall. The outbreak, initially primed by dendritic cells (DC), [...] Read more.
Large-vessel vasculitis (LVV) are autoimmune and autoinflammatory diseases focused on vascular inflammation. The central core of the intricate immunological and molecular network resides in the disruption of the “privileged immune state” of the arterial wall. The outbreak, initially primed by dendritic cells (DC), is then continuously powered in a feed-forward loop by the intimate cooperation between innate and adaptive immunity. If the role of adaptive immunity has been largely elucidated, knowledge of the critical function of innate immunity in LVV is still fragile. A growing body of evidence has strengthened the active role of innate immunity players and their key signaling pathways in orchestrating the complex pathomechanisms underlying LVV. Besides DC, macrophages are crucial culprits in LVV development and participate across all phases of vascular inflammation, culminating in vessel wall remodeling. In recent years, the variety of potential pathogenic actors has expanded to include neutrophils, mast cells, and soluble mediators, including the complement system. Interestingly, new insights have recently linked the inflammasome to vascular inflammation, paving the way for its potential pathogenic role in LVV. Overall, these observations encourage a new conceptual approach that includes a more in-depth study of innate immunity pathways in LVV to guide future targeted therapies. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms Underlying Large-Vessel Vasculitis)
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17 pages, 1132 KiB  
Review
Giant Cell Arteritis: Advances in Understanding Pathogenesis and Implications for Clinical Practice
by Marino Paroli, Rosalba Caccavale and Daniele Accapezzato
Cells 2024, 13(3), 267; https://doi.org/10.3390/cells13030267 - 31 Jan 2024
Cited by 1 | Viewed by 1429
Abstract
Giant cell arteritis (GCA) is a noninfectious granulomatous vasculitis of unknown etiology affecting individuals older than 50 years. Two forms of GCA have been identified: a cranial form involving the medium-caliber temporal artery causing temporal arteritis (TA) and an extracranial form involving the [...] Read more.
Giant cell arteritis (GCA) is a noninfectious granulomatous vasculitis of unknown etiology affecting individuals older than 50 years. Two forms of GCA have been identified: a cranial form involving the medium-caliber temporal artery causing temporal arteritis (TA) and an extracranial form involving the large vessels, mainly the thoracic aorta and its branches. GCA generally affects individuals with a genetic predisposition, but several epigenetic (micro)environmental factors are often critical for the onset of this vasculitis. A key role in the pathogenesis of GCA is played by cells of both the innate and adaptive immune systems, which contribute to the formation of granulomas that may include giant cells, a hallmark of the disease, and arterial tertiary follicular organs. Cells of the vessel wall cells, including vascular smooth muscle cells (VSMCs) and endothelial cells, actively contribute to vascular remodeling responsible for vascular stenosis and ischemic complications. This review will discuss new insights into the molecular and cellular pathogenetic mechanisms of GCA, as well as the implications of these findings for the development of new diagnostic biomarkers and targeted drugs that could hopefully replace glucocorticoids (GCs), still the backbone of therapy for this vasculitis. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms Underlying Large-Vessel Vasculitis)
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