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Molecular Regulators of Cardiovascular Disease

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 June 2023) | Viewed by 5076

Special Issue Editor


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Guest Editor
Department of Anesthesiology, Amsterdam UMC, VU University, 1081 HV Amsterdam, The Netherlands
Interests: cardioprotection; endothelial function

Special Issue Information

Dear Colleagues,

Endotheliopathy plays a role in of the development of organ failure in critically ill patients. During hyperinflammatory conditions that can occur in acute critical illness, such as shock or hypoperfusion, inflammatory mediators activate the endothelium, fueling a proinflammatory host response and procoagulant processes. These changes result in shedding of the glycocalyx, endothelial hyperpermeability and edema formation, and can lead to disturbed microcirculatory perfusion and organ failure. Targeting the endothelium may be a therapeutic strategy to limit organ failure, which hitherto has not received much attention.

Although therapeutic targeting of several molecular pathways seems promising in terms of restoring the endothelium in critical illness, only minor treatments have made it to the clinic. Therefore, more studies are required in order for us to understand the development of endotheliopathy and to improve therapeutic strategies.

We invite scientists and researchers to contribute original research and review articles which provide insight into (new) molecular mechanisms related to the regulation of the endothelium and the development of endotheliopathy.

Dr. Charissa E. Van Den Brom
Guest Editor

Manuscript Submission Information

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Keywords

  • endotheliopathy
  • criticall illness
  • microcirculation
  • molecular mechanism
  • coagulation
  • endothelial barrier function
  • glycocalyx
  • edema
  • organ injury

Published Papers (2 papers)

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Research

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15 pages, 1114 KiB  
Article
Cerebral Blood Flow in Predator Stress-Resilient and -Susceptible Rats and Mechanisms of Resilience
by Marina V. Kondashevskaya, H. Fred Downey, Vadim E. Tseilikman, Valery V. Alexandrin, Kseniya A. Artem’yeva, Valentina V. Aleksankina, Olga B. Tseilikman, Anton A. Pashkov, Anna V. Goryacheva, Irina S. Ivleva, Marina N. Karpenko, Vladislav A. Shatilov and Eugenia B. Manukhina
Int. J. Mol. Sci. 2022, 23(23), 14729; https://doi.org/10.3390/ijms232314729 - 25 Nov 2022
Cited by 3 | Viewed by 2124
Abstract
Stress-induced conditions are associated with impaired cerebral blood flow (CBF) and increased risk of dementia and stroke. However, these conditions do not develop in resilient humans and animals. Here the effects of predator stress (PS, cat urine scent, ten days) on CBF and [...] Read more.
Stress-induced conditions are associated with impaired cerebral blood flow (CBF) and increased risk of dementia and stroke. However, these conditions do not develop in resilient humans and animals. Here the effects of predator stress (PS, cat urine scent, ten days) on CBF and mechanisms of CBF regulation were compared in PS-susceptible (PSs) and PS-resilient (PSr) rats. Fourteen days post-stress, the rats were segregated into PSs and PSr groups based on a behavior-related anxiety index (AI). CBF and its endothelium-dependent changes were measured in the parietal cortex by laser Doppler flowmetry. The major findings are: (1) PS susceptibility was associated with reduced basal CBF and endothelial dysfunction. In PSr rats, the basal CBF was higher, and endothelial dysfunction was attenuated. (2) CBF was inversely correlated with the AI of PS-exposed rats. (3) Endothelial dysfunction was associated with a decrease in eNOS mRNA in PSs rats compared to the PSr and control rats. (4) Brain dopamine was reduced in PSs rats and increased in PSr rats. (5) Plasma corticosterone of PSs was reduced compared to PSr and control rats. (6) A hypercoagulation state was present in PSs rats but not in PSr rats. Thus, potential stress resilience mechanisms that are protective for CBF were identified. Full article
(This article belongs to the Special Issue Molecular Regulators of Cardiovascular Disease)
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Review

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17 pages, 3018 KiB  
Review
Significance of Intra-plaque Hemorrhage for the Development of High-Risk Vulnerable Plaque: Current Understanding from Basic to Clinical Points of View
by Atsushi Sakamoto, Kenichiro Suwa, Rika Kawakami, Alexandra V. Finn, Yuichiro Maekawa, Renu Virmani and Aloke V. Finn
Int. J. Mol. Sci. 2023, 24(17), 13298; https://doi.org/10.3390/ijms241713298 - 27 Aug 2023
Cited by 4 | Viewed by 2428
Abstract
Acute coronary syndromes due to atherosclerotic coronary artery disease are a leading cause of morbidity and mortality worldwide. Intra-plaque hemorrhage (IPH), caused by disruption of intra-plaque leaky microvessels, is one of the major contributors of plaque progression, causing a sudden increase in plaque [...] Read more.
Acute coronary syndromes due to atherosclerotic coronary artery disease are a leading cause of morbidity and mortality worldwide. Intra-plaque hemorrhage (IPH), caused by disruption of intra-plaque leaky microvessels, is one of the major contributors of plaque progression, causing a sudden increase in plaque volume and eventually plaque destabilization. IPH and its healing processes are highly complex biological events that involve interactions between multiple types of cells in the plaque, including erythrocyte, macrophages, vascular endothelial cells and vascular smooth muscle cells. Recent investigations have unveiled detailed molecular mechanisms by which IPH leads the development of high-risk “vulnerable” plaque. Current advances in clinical diagnostic imaging modalities, such as magnetic resonance image and intra-coronary optical coherence tomography, increasingly allow us to identify IPH in vivo. To date, retrospective and prospective clinical trials have revealed the significance of IPH as detected by various imaging modalities as a reliable prognostic indicator of high-risk plaque. In this review article, we discuss recent advances in our understanding for the significance of IPH on the development of high-risk plaque from basic to clinical points of view. Full article
(This article belongs to the Special Issue Molecular Regulators of Cardiovascular Disease)
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