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Biomedicines
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Microcirculation, Thrombosis, and Inflammation in Peripheral Artery Disease and in...
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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: 28 February 2026 | Viewed by 2748

Special Issue Editors

Dr. Patricia Pia Wadowski

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals
Dr. Henriette Löffler-Stastka

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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 (3 papers)

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Research

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10 pages, 1093 KB  
Article
Microvascular Density Analysis of Patients with Trigeminal Herpes Zoster—An Optical Coherence Tomography Angiography Study
by Eliane Luisa Esser, Steven Brozmann, Sebastian Dierse, Martin Dominik Leclaire, Nicole Eter, Nataša Mihailovic and Jan Ehrchen
Biomedicines 2025, 13(7), 1630; https://doi.org/10.3390/biomedicines13071630 - 3 Jul 2025
Cited by 1 | Viewed by 745
Abstract
Purpose: Varicella zoster virus (VZV) vasculopathy can occur in patients with herpes zoster (HZ). Our aim was to evaluate the retinal microvascular vessel density (VD) in patients with trigeminal HZ measured by optical coherence tomography angiography (OCTA). Methods: 48 eyes of 24 [...] Read more.
Purpose: Varicella zoster virus (VZV) vasculopathy can occur in patients with herpes zoster (HZ). Our aim was to evaluate the retinal microvascular vessel density (VD) in patients with trigeminal HZ measured by optical coherence tomography angiography (OCTA). Methods: 48 eyes of 24 patients with HZ and 48 eyes of 24 healthy age- and gender-matched controls were included in this study. All participants underwent an OCTA examination using RTVue XR Avanti with AngioVue. The VD data of the macular 3 × 3 mm OCT angiogram of the superficial capillary plexus (SCP), the deep capillary plexus (DCP), and the choriocapillaris (CC) as well as the VD data of the optic nerve head (ONH) were extracted and analyzed. Results: The VD in the SCP, DCP, and CC of patients with HZ was significantly lower compared with healthy controls (p < 0.05). Equally, there was a noticeable reduction in the inside disk area of the ONH. There was no statistically noticeable reduction in the FAZ area and central retinal thickness. Conclusions: In this study, HZ patients demonstrated a decrease in the retinal VD of the SCP, DCP, ONH, and the CC. Quantitative analysis of retinal perfusion using OCTA may therefore help in the diagnosis and monitoring of HZ. Further studies must show to what extent this may be an indication of VZV-related vasculopathy and whether OCTA data can be used as a biomarker in these patients in the future. Full article
(This article belongs to the Special Issue Microcirculation, Thrombosis, and Inflammation in Peripheral Artery Disease and in the Brain)
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16 pages, 1275 KB  
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
(This article belongs to the Special Issue Microcirculation, Thrombosis, and Inflammation in Peripheral Artery Disease and in the Brain)
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Review

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25 pages, 1032 KB  
Review
Microvascular Failure in the Aging Brain: Converging Pathways of Oxidative Stress, Inflammation, and Endothelial Decline
by Jordana Mariane Neyra Chauca, Maclovia Vázquez VanDyck, Armando Espinoza Santana, Graciela Gaddy Robles Martínez, Kalid Alejandra Romero Vega, Nancy García Quintana and Vanessa Favila Sánchez
Biomedicines 2026, 14(1), 130; https://doi.org/10.3390/biomedicines14010130 - 8 Jan 2026
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Abstract
Background: Aging exerts a progressive and multifaceted impact on the microcirculatory system, undermining the structural and molecular integrity that sustains endothelial stability across both peripheral and cerebral vascular territories. A sustained shift toward oxidative imbalance, chronic low-grade inflammation, and progressive endothelial exhaustion [...] Read more.
Background: Aging exerts a progressive and multifaceted impact on the microcirculatory system, undermining the structural and molecular integrity that sustains endothelial stability across both peripheral and cerebral vascular territories. A sustained shift toward oxidative imbalance, chronic low-grade inflammation, and progressive endothelial exhaustion converges to destabilize microvascular networks, linking peripheral artery disease (PAD) with heightened susceptibility to cerebral microvascular dysfunction and neurovascular decline. As redox homeostasis deteriorates, endothelial cells progressively lose barrier-selective properties, intercellular communication with pericytes weakens, and pro-thrombotic tendencies subtly emerge, creating a permissive environment for early neurovascular injury and impaired cerebrovascular resilience. Methods: This narrative review integrates mechanistic evidence derived from experimental, clinical, and translational studies examining the interplay between oxidative stress, inflammatory signaling cascades, endothelial senescence, and blood–brain barrier (BBB) disruption across peripheral and cerebral microvascular systems. A comparative framework was applied to PAD and cerebral microcirculatory pathology to identify convergent molecular drivers and systemic mechanisms underlying endothelial deterioration. Results: Accumulating evidence demonstrates that oxidative stress disrupts endothelial mitochondrial function, compromises tight junction architecture, and accelerates angiogenic failure. Concurrent inflammatory activation amplifies these alterations through cytokine-mediated endothelial activation, enhanced leukocyte adhesion, and promotion of a pro-thrombotic microenvironment. Progressive endothelial senescence consolidates these insults into a persistent state of microvascular dysfunction characterized by diminished nitric oxide bioavailability, capillary rarefaction, and compromised barrier integrity. Notably, these pathological features are shared between PAD and the aging cerebral circulation, reinforcing the concept of a unified systemic microvascular aging phenotype. Conclusions: Microvascular failure in the aging brain should be understood as an extension of systemic endothelial deterioration driven by oxidative stress, chronic inflammation, and senescence-associated vascular exhaustion. Recognizing the shared molecular architecture linking peripheral and cerebral microcirculatory dysfunction offers a strategic framework for developing targeted therapeutic interventions aimed at restoring endothelial resilience, stabilizing BBB integrity, and preserving neurovascular homeostasis in aging populations. Full article
(This article belongs to the Special Issue Microcirculation, Thrombosis, and Inflammation in Peripheral Artery Disease and in the Brain)
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