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Contribution of Dysfunctional Microvasculature to Cardiovascular Diseases
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Contribution of Dysfunctional Microvasculature to Cardiovascular Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 7121

Special Issue Editor

Dr. Margreet de Vries

E-Mail Website
Guest Editor
Department of Surgery, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands
Interests: vascular diseases; vein graft disease; arteriovenous fistula failure; arteriovenous fistula; vascular inflammation; AVF maturation; vascular remodeling; angiogenesis; ultrasound; photoacoustics

Special Issue Information

Dear Colleagues,

Microvascular endothelium is crucial for the oxygenation and nutrition of tissues. The integrity and barrier function of the endothelium is maintained by intercellular junctions. However, when microvascular endothelial cells become dysfunctional, a decreased barrier function will occur. Activation of the endothelium by damage- or pathogen-associated molecular patterns (DAMPs/PAMPs), disturbed flow, Ox-LDL, or decreased nitic oxide causes upregulation of adhesion molecules such as ICAM-1 and VCAM-1 and NF-κB mediated cytokine expression. Upon dysfunction, fluids, ions, and cells can cross the endothelium and leak into the underlying extracellular matrix, causing inflammation and negatively affecting the blood vessel wall and cardiovascular disease progression.

This Special Issue of the International Journal of Molecular Sciences focuses on the contribution of dysfunctional microvasculature to inflammation, cardiovascular diseases, and other pathologies and welcomes both original research articles and review papers that deal with the molecular mechanisms underlying the role of microvascular dysfunction.

Dr. Margreet de Vries
Guest Editor

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Keywords

  • endothelial cells
  • angiogenesis
  • leukocyte transmigration
  • intercellular junctions
  • hemorrhage
  • inflammation
  • leaky neovessels
  • barrier function

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Published Papers (3 papers)

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Research

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20 pages, 2139 KiB  
Article
Effects of Gender and Vitamin D on Vascular Reactivity of the Carotid Artery on a Testosterone-Induced PCOS Model
by Anita Süli, Péter Magyar, Márton Vezér, Bálint Bányai, Mária Szekeres, Miklós Sipos, Máté Mátrai, Judit Réka Hetthéssy, Gabriella Dörnyei, Nándor Ács, Eszter Mária Horváth, György L. Nádasy, Szabolcs Várbíró and Marianna Török
Int. J. Mol. Sci. 2023, 24(23), 16577; https://doi.org/10.3390/ijms242316577 - 21 Nov 2023
Viewed by 1727
Abstract
The negative cardiovascular effects of polycystic ovary syndrome (PCOS) and vitamin D deficiency (VDD) have been discussed previously; however, the sex differences between PCOS females and males are not yet known. Our aim was to investigate the effect of PCOS and VDD in [...] Read more.
The negative cardiovascular effects of polycystic ovary syndrome (PCOS) and vitamin D deficiency (VDD) have been discussed previously; however, the sex differences between PCOS females and males are not yet known. Our aim was to investigate the effect of PCOS and VDD in the carotid artery of male and female Wistar rats. Females were treated with transdermal testosterone (Androgel) for 8 weeks, which caused PCOS. VDD and vitamin D supplementation were accomplished via diet. The carotid arteries’ contraction and relaxation were examined using myography. Receptor density was investigated using immunohistochemistry. In PCOS females, angiotensin receptor density, angiotensin II-induced contraction, androgen receptor optical density, and testosterone-induced relaxation increased. The increased contractile response may increase cardiovascular vulnerability in women with PCOS. As an effect of VDD, estrogen receptor density increased in all our groups, which probably compensated for the reduced relaxation caused by VDD. Testosterone-induced relaxation was decreased as a result of VDD in males and non-PCOS females, whereas this reduction was absent in PCOS females. Male sex is associated with increased contraction ability compared with non-PCOS and PCOS females. VDD and Androgel treatment show significant gender differences in their effects on carotid artery reactivity. Both VDD and PCOS result in a dysfunctional vascular response, which can contribute to cardiovascular diseases. Full article
(This article belongs to the Special Issue Contribution of Dysfunctional Microvasculature to Cardiovascular Diseases)
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16 pages, 40300 KiB  
Article
Phosphorylcholine Monoclonal Antibody Therapy Decreases Intraplaque Angiogenesis and Intraplaque Hemorrhage in Murine Vein Grafts
by Fabiana Baganha, Thijs J. Sluiter, Rob C. M. de Jong, Louise A. van Alst, Hendrika A. B. Peters, J. Wouter Jukema, Mirela Delibegovic, Knut Pettersson, Paul H. A. Quax and Margreet R. de Vries
Int. J. Mol. Sci. 2022, 23(21), 13662; https://doi.org/10.3390/ijms232113662 - 7 Nov 2022
Cited by 3 | Viewed by 2751
Abstract
Phosphorylcholine (PC) is one of the main oxLDL epitopes playing a central role in atherosclerosis, due to its atherogenic and proinflammatory effects. PC can be cleared by natural IgM antibodies and low levels of these antibodies have been associated with human vein graft [...] Read more.
Phosphorylcholine (PC) is one of the main oxLDL epitopes playing a central role in atherosclerosis, due to its atherogenic and proinflammatory effects. PC can be cleared by natural IgM antibodies and low levels of these antibodies have been associated with human vein graft (VG) failure. Although PC antibodies are recognized for their anti-inflammatory properties, their effect on intraplaque angiogenesis (IPA) and intraplaque hemorrhage (IPH)—interdependent processes contributing to plaque rupture—are unknown. We hypothesized that new IgG phosphorylcholine antibodies (PC-mAb) could decrease vulnerable lesions in murine VGs.Therefore, hypercholesterolemic male ApoE3*Leiden mice received a (donor) caval vein interposition in the carotid artery and weekly IP injections of (5 mg/kg) PCmAb (n = 11) or vehicle (n = 12) until sacrifice at day 28. We found that PCmAb significantly decreased vein graft media (13%), intima lesion (25%), and increased lumen with 32% compared to controls. PCmAb increased collagen content (18%) and decreased macrophages presence (31%). PCmAb resulted in 23% decreased CD163+ macrophages content in vein grafts whereas CD163 expression was decreased in Hb:Hp macrophages. PCmAb significantly lowered neovessel density (34%), EC proliferation and migration with/out oxLDL stimulation. Moreover, PCmAb enhanced intraplaque angiogenic vessels maturation by increasing neovessel pericyte coverage in vivo (31%). Together, this resulted in a 62% decrease in IPH. PCmAb effectively inhibits murine atherosclerotic lesion formation in vein grafts by reducing IPA and IPH via decreased neovessel density and macrophages influx and increased neovessel maturation. PC-mAb therefore holds promise as a new therapeutic approach to prevent vein graft disease. Full article
(This article belongs to the Special Issue Contribution of Dysfunctional Microvasculature to Cardiovascular Diseases)
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Review

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28 pages, 3519 KiB  
Review
Clinical Potential of Hydrogen Sulfide in Peripheral Arterial Disease
by Clémence Bechelli, Diane Macabrey, Sebastien Deglise and Florent Allagnat
Int. J. Mol. Sci. 2023, 24(12), 9955; https://doi.org/10.3390/ijms24129955 - 9 Jun 2023
Cited by 5 | Viewed by 2002
Abstract
Peripheral artery disease (PAD) affects more than 230 million people worldwide. PAD patients suffer from reduced quality of life and are at increased risk of vascular complications and all-cause mortality. Despite its prevalence, impact on quality of life and poor long-term clinical outcomes, [...] Read more.
Peripheral artery disease (PAD) affects more than 230 million people worldwide. PAD patients suffer from reduced quality of life and are at increased risk of vascular complications and all-cause mortality. Despite its prevalence, impact on quality of life and poor long-term clinical outcomes, PAD remains underdiagnosed and undertreated compared to myocardial infarction and stroke. PAD is due to a combination of macrovascular atherosclerosis and calcification, combined with microvascular rarefaction, leading to chronic peripheral ischemia. Novel therapies are needed to address the increasing incidence of PAD and its difficult long-term pharmacological and surgical management. The cysteine-derived gasotransmitter hydrogen sulfide (H2S) has interesting vasorelaxant, cytoprotective, antioxidant and anti-inflammatory properties. In this review, we describe the current understanding of PAD pathophysiology and the remarkable benefits of H2S against atherosclerosis, inflammation, vascular calcification, and other vasculo-protective effects. Full article
(This article belongs to the Special Issue Contribution of Dysfunctional Microvasculature to Cardiovascular Diseases)
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