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Peripheral Artery Disease: Inflammatory, Metabolic and Coagulative Pathogenetic Implications
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Peripheral Artery Disease: Inflammatory, Metabolic and Coagulative Pathogenetic Implications

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

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 7340

Special Issue Editors

Prof. Dr. Antonino Tuttolomondo

E-Mail Website
Guest Editor
Biomedical Department of Internal Medicine and Medical Specialties (Di.Bi.M.I.S), University of Palermo, 90133 Palermo, Italy
Interests: ischemic stroke in diabetes; diabetic foot; Anderson-Fabry disease; cytokines
Special Issues, Collections and Topics in MDPI journals
Dr. Giuseppe Miceli

E-Mail Website
Co-Guest Editor
Department of Scienze per la promozione della Salute “G. D’Alessandro”, Università degli Studi di Palermo, 90127 Palermo, Italy
Interests: peripheral artery disease; neurosonology; atherosclerosis; transcranial doppler; cerebral hemodynamic
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Peripheral arterial disease (PAD) is an atherosclerotic-based disease with a large-scale impact on economy and global health. Different hemodynamic, metabolic, inflammatory, and oxidative mechanisms are involved in the pathophysiology of PAD.

The equilibrium between proatherogenic inflammatory and atheroprotective anti-inflammatory signals is regulated by a complex network of pathways involving the endothelium components and several immune cells such as macrophages, monocytes and T, B, and foam cells.  These cell and molecular interactions, not yet fully elucidated, can be responsible for the further progression and instability of the atherosclerotic lesions and for the accelerated functional decline in PAD patients. Moreover, metabolomic profile and the levels of several lipids and fat related markers have also been implicated in PAD severity and progression.

Finally, evidence is accumulating that the inflammatory and coagulation pathways play an important role in atherogenesis, plaque instability and atherothrombotic complications with future potential therapeutic implications. This Special Issue attempts to investigate the role of novel inflammatory, metabolic and coagulative mechanisms in PAD. This Special Issue welcomes original research or review papers that have the objective to elucidate the inflammatory, metabolic and coagulative interactions in the complex pathophysiological scenario of PAD. 

Prof. Dr. Antonino Tuttolomondo
Dr. Giuseppe Miceli
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. 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

  • peripheral artery disease
  • inflammation
  • atherogenesis

Published Papers (3 papers)

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Review

18 pages, 672 KiB  
Review
Inflammatory, Metabolic, and Coagulation Effects on Medial Arterial Calcification in Patients with Peripheral Arterial Disease
by Jovana Nikolajević and Mišo Šabovič
Int. J. Mol. Sci. 2023, 24(4), 3132; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24043132 - 05 Feb 2023
Cited by 3 | Viewed by 2010
Abstract
Calcium deposits in the vessel wall in the form of hydroxyapatite can accumulate in the intimal layer, as in atherosclerotic plaque, but also in the medial layer, as in medial arterial calcification (MAC) or medial Möenckeberg sclerosis. Once considered a passive, degenerative process, [...] Read more.
Calcium deposits in the vessel wall in the form of hydroxyapatite can accumulate in the intimal layer, as in atherosclerotic plaque, but also in the medial layer, as in medial arterial calcification (MAC) or medial Möenckeberg sclerosis. Once considered a passive, degenerative process, MAC has recently been shown to be an active process with a complex but tightly regulated pathophysiology. Atherosclerosis and MAC represent distinct clinical entities that correlate in different ways with conventional cardiovascular risk factors. As both entities coexist in the vast majority of patients, it is difficult to estimate the relative contribution of specific risk factors to their development. MAC is strongly associated with age, diabetes mellitus, and chronic kidney disease. Given the complexity of MAC pathophysiology, it is expected that a variety of different factors and signaling pathways may be involved in the development and progression of the disease. In this article, we focus on metabolic factors, primarily hyperphosphatemia and hyperglycemia, and a wide range of possible mechanisms by which they might contribute to the development and progression of MAC. In addition, we provide insight into possible mechanisms by which inflammatory and coagulation factors are involved in vascular calcification processes. A better understanding of the complexity of MAC and the mechanisms involved in its development is essential for the development of potential preventive and therapeutic strategies. Full article
(This article belongs to the Special Issue Peripheral Artery Disease: Inflammatory, Metabolic and Coagulative Pathogenetic Implications)
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31 pages, 892 KiB  
Review
The Role of the Coagulation System in Peripheral Arterial Disease: Interactions with the Arterial Wall and Its Vascular Microenvironment and Implications for Rational Therapies
by Giuseppe Miceli, Maria Grazia Basso, Giuliana Rizzo, Chiara Pintus and Antonino Tuttolomondo
Int. J. Mol. Sci. 2022, 23(23), 14914; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232314914 - 29 Nov 2022
Cited by 7 | Viewed by 2865
Abstract
Peripheral artery disease (PAD) is a clinical manifestation of atherosclerotic disease with a large-scale impact on the economy and global health. Despite the role played by platelets in the process of atherogenesis being well recognized, evidence has been increasing on the contribution of [...] Read more.
Peripheral artery disease (PAD) is a clinical manifestation of atherosclerotic disease with a large-scale impact on the economy and global health. Despite the role played by platelets in the process of atherogenesis being well recognized, evidence has been increasing on the contribution of the coagulation system to the atherosclerosis formation and PAD development, with important repercussions for the therapeutic approach. Histopathological analysis and some clinical studies conducted on atherosclerotic plaques testify to the existence of different types of plaques. Likely, the role of coagulation in each specific type of plaque can be an important determinant in the histopathological composition of atherosclerosis and in its future stability. In this review, we analyze the molecular contribution of inflammation and the coagulation system on PAD pathogenesis, focusing on molecular similarities and differences between atherogenesis in PAD and coronary artery disease (CAD) and discussing the possible implications for current therapeutic strategies and future perspectives accounting for molecular inflammatory and coagulation targets. Understanding the role of cross-talking between coagulation and inflammation in atherosclerosis genesis and progression could help in choosing the right patients for future dual pathway inhibition strategies, where an antiplatelet agent is combined with an anticoagulant, whose role, despite pathophysiological premises and trials’ results, is still under debate. Full article
(This article belongs to the Special Issue Peripheral Artery Disease: Inflammatory, Metabolic and Coagulative Pathogenetic Implications)
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32 pages, 1048 KiB  
Review
The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine
by Lăcrămioara Ionela Butnariu, Eusebiu Vlad Gorduza, Laura Florea, Elena Țarcă, Ștefana Maria Moisă, Laura Mihaela Tradafir, Elena Cojocaru, Alina-Costina Luca, Laura Stătescu and Minerva Codruța Bădescu
Int. J. Mol. Sci. 2022, 23(18), 10481; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231810481 - 09 Sep 2022
Cited by 2 | Viewed by 2082
Abstract
Lower extremity artery disease (LEAD), caused by atherosclerotic obstruction of the arteries of the lower limb extremities, has exhibited an increase in mortality and morbidity worldwide. The phenotypic variability of LEAD is correlated with its complex, multifactorial etiology. In addition to traditional risk [...] Read more.
Lower extremity artery disease (LEAD), caused by atherosclerotic obstruction of the arteries of the lower limb extremities, has exhibited an increase in mortality and morbidity worldwide. The phenotypic variability of LEAD is correlated with its complex, multifactorial etiology. In addition to traditional risk factors, it has been shown that the interaction between genetic factors (epistasis) or between genes and the environment potentially have an independent role in the development and progression of LEAD. In recent years, progress has been made in identifying genetic variants associated with LEAD, by Genome-Wide Association Studies (GWAS), Whole Exome Sequencing (WES) studies, and epigenetic profiling. The aim of this review is to present the current knowledge about the genetic factors involved in the etiopathogenic mechanisms of LEAD, as well as possible directions for future research. We analyzed data from the literature, starting with candidate gene-based association studies, and then continuing with extensive association studies, such as GWAS and WES. The results of these studies showed that the genetic architecture of LEAD is extremely heterogeneous. In the future, the identification of new genetic factors will allow for the development of targeted molecular therapies, and the use of polygenic risk scores (PRS) to identify individuals at an increased risk of LEAD will allow for early prophylactic measures and personalized therapy to improve their prognosis. Full article
(This article belongs to the Special Issue Peripheral Artery Disease: Inflammatory, Metabolic and Coagulative Pathogenetic Implications)
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