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Inflammatory Disturbances in Cerebrovascular and Cardiovascular Diseases
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Inflammatory Disturbances in Cerebrovascular and Cardiovascular Diseases

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

Deadline for manuscript submissions: 30 April 2024 | Viewed by 2466

Special Issue Editors

Dr. Helena Kim

E-Mail Website
Guest Editor
School of Agriculture, Biomedicine & Environment, La Trobe University, Melbourne, VIC 3086, Australia
Interests: cerebrovascular disease
Prof. Dr. Chris Sobey

E-Mail Website
Guest Editor
Department of Physiology, Anatomy & Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC, Australia
Interests: cardiovascular disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD) is the leading cause of death globally, taking an estimated 17 million lives each year. Approximately 80% of CVD deaths are due to heart attacks and stroke. Inflammation constitutes a hallmark of CVD development and contributes to atherosclerosis, myocardial infarction, heart failure, and hypertension. A rich body of literature demonstrates that acute or chronic inflammation is associated with the increased risk of CVD and may be an important determinant of outcomes. Indeed, post-stroke inflammation and immunodepression may increase the risk of infections such as pneumonia and negatively impact the disease outcome. Immunomodulatory approaches to managing multiple CVDs are gaining interest. The main objective of this Special Issue is to enhance our basic understanding by identifying novel targets and mechanisms of inflammatory disturbances in CVD. Potential study topics include, but are not limited to, immune target identification, models of immune cell deletion, immunomodulatory therapy, and the spatiotemporal distribution of immune cells and cytokines/chemokine in the context of CVDs.

Dr. Helena Kim
Prof. Dr. Chris Sobey
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

  • cardiovascular disease
  • cerebrovascular disease
  • acute or chronic inflammation
  • neuroinflammation
  • cytokines/chemokines
  • immune therapy
  • immunomodulation
  • stroke
  • atherosclerosis
  • hypertension
  • heart failure

Published Papers (2 papers)

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Research

15 pages, 1464 KiB  
Article
Oxidative Stress and Antioxidant Defense Mechanisms in Acute Ischemic Stroke Patients with Concurrent COVID-19 Infection
by Elena Anca Pinoșanu, Roxana Surugiu, Emilia Burada, Denisa Pîrșcoveanu, Camelia Elena Stănciulescu, Raluca Elena Sandu, Cătălina Pisoschi and Carmen Valeria Albu
Int. J. Mol. Sci. 2023, 24(23), 16790; https://doi.org/10.3390/ijms242316790 - 27 Nov 2023
Viewed by 973
Abstract
Stroke remains a debilitating cerebrovascular condition associated with oxidative stress, while COVID-19 has emerged as a global health crisis with multifaceted systemic implications. This study investigates the hypothesis that patients experiencing acute ischemic stroke alongside COVID-19 exhibit elevated oxidative stress markers and altered [...] Read more.
Stroke remains a debilitating cerebrovascular condition associated with oxidative stress, while COVID-19 has emerged as a global health crisis with multifaceted systemic implications. This study investigates the hypothesis that patients experiencing acute ischemic stroke alongside COVID-19 exhibit elevated oxidative stress markers and altered antioxidant defense mechanisms compared to those with acute ischemic stroke. We conducted a single-center prospective cross-sectional study to investigate oxidative stress balance through oxidative damage markers: TBARS (thiobarbituric acid reactive substances level) and PCARB (protein carbonyls); antioxidant defense mechanisms: TAC (total antioxidant capacity), GPx (glutathione peroxidase), GSH (reduced glutathione), CAT (catalase), and SOD (superoxide dismutase); as well as inflammatory response markers: NLR (neutrophil-to-lymphocyte ratio), CRP (C-reactive protein), and ESR (erythrocyte sedimentation rate). Statistical analyses and correlation models were employed to elucidate potential associations and predictive factors. Our results revealed increased oxidative stress, predominantly indicated by elevated levels of TBARS in individuals experiencing ischemic stroke alongside a concurrent COVID-19 infection (p < 0.0001). The Stroke-COVID group displayed notably elevated levels of GSH (p = 0.0139 *), GPx (p < 0.0001 ****), SOD (p = 0.0363 *), and CAT (p = 0.0237 *) activities. Multivariate analysis found a significant association for TBARS (p < 0.0001 ****), PCARB (p = 0.0259 *), and GPx activity (p < 0.0001 ****), together with NLR (p = 0.0220 *) and CRP (p = 0.0008 ***). Notably, the interplay between stroke and COVID-19 infection appears to amplify oxidative damage, potentially contributing to exacerbated neurological deficits and poorer outcomes. This study highlights the intricate relationship between oxidative stress, inflammation, and concurrent health conditions. Understanding these interactions may open avenues for novel therapeutic strategies aimed at ameliorating oxidative damage in patients with acute ischemic stroke and COVID-19, ultimately improving their prognosis and quality of life. Full article
(This article belongs to the Special Issue Inflammatory Disturbances in Cerebrovascular and Cardiovascular Diseases)
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8 pages, 1546 KiB  
Communication
Dimethyl Fumarate Attenuates Lymphocyte Infiltration and Reduces Infarct Size in Experimental Stroke
by Michael K. Schuhmann, Friederike Langhauser, Lena Zimmermann, Maximilian Bellut, Christoph Kleinschnitz and Felix Fluri
Int. J. Mol. Sci. 2023, 24(21), 15540; https://doi.org/10.3390/ijms242115540 - 24 Oct 2023
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Abstract
Ischemic stroke is associated with exacerbated tissue damage caused by the activation of immune cells and the initiation of other inflammatory processes. Dimethyl fumarate (DMF) is known to modulate the immune response, activate antioxidative pathways, and improve the blood–brain barrier (BBB) after stroke. [...] Read more.
Ischemic stroke is associated with exacerbated tissue damage caused by the activation of immune cells and the initiation of other inflammatory processes. Dimethyl fumarate (DMF) is known to modulate the immune response, activate antioxidative pathways, and improve the blood–brain barrier (BBB) after stroke. However, the specific impact of DMF on immune cells after cerebral ischemia remains unclear. In our study, male mice underwent transient middle cerebral artery occlusion (tMCAO) for 30 min and received oral DMF (15 mg/kg) or a vehicle immediately after tMCAO, followed by twice-daily administrations for 7 days. Infarct volume was assessed on T2-weighted magnetic resonance images on days 1 and 7 after tMCAO. Brain-infiltrating immune cells (lymphocytes, monocytes) and microglia were quantified using fluorescence-activated cell sorting. DMF treatment significantly reduced infarct volumes and brain edema. On day 1 after tMCAO, DMF-treated mice showed reduced lymphocyte infiltration compared to controls, which was not observed on day 7. Monocyte and microglial cell counts did not differ between groups on either day. In the acute phase of stroke, DMF administration attenuated lymphocyte infiltration, probably due to its stabilizing effect on the BBB. This highlights the potential of DMF as a therapeutic candidate for mitigating immune cell-driven damage in stroke. Full article
(This article belongs to the Special Issue Inflammatory Disturbances in Cerebrovascular and Cardiovascular Diseases)
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