Microcirculation, Thrombosis, and Inflammation in Peripheral Artery Disease and in the Brain

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 627

Special Issue Editors


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Guest Editor
Department of Internal Medicine II, Division of Angiology, Medical University of Vienna, 1090 Wien, Austria
Interests: platelets; pharmacology; microcirculation; glycocalyx; thrombosis and hemostasis
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Co-Guest Editor
Department of Psychoanalysis and Psychotherapy, Medical University of Vienna, 1090 Vienna, Austria
Interests: psychotherapy research and training research; therapist variable; psychotherapy/psychoanalysis with severely disturbed patients; psychotic disorders; health care management
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Special Issue Information

Dear Colleagues,

Peripheral artery disease is, to a wide extent, driven by chronic inflammatory and prothrombotic signaling pathways. Vascular dysfunction underlies the progression of atherosclerosis and macrovascular as well as microvascular alterations. Moreover, pro-inflammatory signaling pathways are supposed to be a link between atherosclerotic and neuropsychological diseases. The same inflammatory pathways, especially proinflammatory cytokines, are also discussed as potential factors for alterations in synaptic plasticity, signal intensity, and functional connectivity of the brain, with a potentially important role for the microglia. The difference is that in neuroinflammation, no broad invasion into tissue or tissue destruction takes place. Instead, functional connectivity problems or neurotransmitter alterations, for example, lead to clinically similar pictures as psychic alterations due to artery disease. Only precise differentiation in clinical diagnosis, e.g., concerning affect regulation problems, helps to differentiate and provide proper treatment. This Special Issue invites us to dig into the biomedical exploration of these differentiations and enrich the bio-psycho connection. We welcome articles focusing on peripheral artery disease, including vascular dysfunction, thrombosis, and inflammation, with a special focus on the context of systemic secretion of chemokines and neurotransmitter alterations.

Dr. Patricia Pia Wadowski
Dr. Henriette Löffler-Stastka
Guest Editors

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Keywords

  • microcirculation
  • thrombosis
  • inflammation
  • peripheral artery disease
  • brain

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Published Papers (1 paper)

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Research

16 pages, 1275 KiB  
Article
Cholinesterase and Inflammation: Exploring Its Role and Associations with Inflammatory Markers in Patients with Lower Extremity Artery Disease
by Maximilian Mitteregger, Sabine Steiner, Andrea Willfort-Ehringer, Thomas Gremmel, Renate Koppensteiner, Michael Gschwandtner, Eva-Luise Ritter-Hobl, Christoph W. Kopp and Patricia P. Wadowski
Biomedicines 2025, 13(4), 823; https://doi.org/10.3390/biomedicines13040823 - 30 Mar 2025
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Abstract
Background: Inflammation is a major driver of atherosclerotic diseases including lower extremity artery disease (LEAD). Serum cholinesterase (ChE) has been shown to impact cardiovascular health and regulate inflammatory processes. Objectives: The aim of this study was to investigate the relationship between serum ChE [...] Read more.
Background: Inflammation is a major driver of atherosclerotic diseases including lower extremity artery disease (LEAD). Serum cholinesterase (ChE) has been shown to impact cardiovascular health and regulate inflammatory processes. Objectives: The aim of this study was to investigate the relationship between serum ChE levels and inflammatory markers in patients with hemodynamically relevant iliac artery stenosis, assessing its potential role in the inflammatory processes of lower extremity artery disease (LEAD). Methods: In the following retrospective data analysis, we investigated 150 patients with hemodynamically relevant iliac artery stenosis as documented by a delta peak systolic velocity (δPSV) ≥ 1.4 m/s and investigated the possible influence of ChE on established inflammatory markers, such as neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and hemoglobin-to-platelet ratio (HPR), along with other routine laboratory or vascular parameters. Results: ChE levels differed significantly between patients with stable claudication (Fontaine stage II) and critical ischemia (Fontaine stages III and IV): 7.76 mg/dL (6.55–8.7 mg/dL) vs. 6.77 mg/dL (5.85–7.48 mg/dL), p = 0.004. Using the spearman correlation coefficient, testing of NLR and ChE revealed a highly significant inverse correlation, with a coefficient of −0.303 (p < 0.001). Additionally, a weak inverse correlation was observed between PLR and ChE, with a coefficient of −0.162 (p = 0.049). Patients with an elevated body mass index (BMI) showed increased levels of serum ChE, with a spearman correlation coefficient of 0.298 (p < 0.001). Conclusions: The observed correlations in this study depict active inflammation in LEAD with an emphasis on patients with critical ischemia. Serum ChE could serve as a potential biomarker for inflammation in patients with LEAD, particularly in distinguishing between stable claudication and critical ischemia. Future research is needed to explore the role of ChE as a complementary biomarker, offering insights into the cholinergic regulation of inflammation in LEAD. Full article
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