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Endothelial Dysfunction and Cardiovascular Diseases

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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: 25 July 2024 | Viewed by 2826

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Special Issue Editor

Dr. Olga Kruszelnicka

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Guest Editor

Department of Coronary Artery Disease and Heart Failure, Jagiellonian University Medical College, 80 Prądnicka Street, 31-202 Cracow, Poland
Interests: endothelium dysfunction in 2 type diabetes; coronary artery disease and valvular disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

With a particular focus on molecular-level research, we plan to delve into endothelial function in cardiovascular diseases. The vascular endothelium—covering a surface of more than 1000 m²—plays a crucial role in both damage and repair events within the cardiovascular system. The on-going balance between endothelial injury and regeneration is not only linked to the risk of acute coronary syndromes, but also modulates the long-term remodeling of the heart and vessel wall. Activated endothelial cells can express adhesion molecules and secrete leukocyte-attracting chemokines. A complex interplay of the endothelium and leukocyte trafficking has a potential to contribute to the pathogenesis of a variety of diseases. Additionally, a deficient bioavailability of endothelial mediators, nitric oxide and prostacyclin triggers the activation of platelets that liberate leukocyte-attracting chemokines, which links hemostasis to immunity and inflammation. The aim of our Special Issue is to get a deeper insight into the molecular pathways involved in a cross-talk between leukocyte-derived cytokines and endothelial or platelet chemokines implicated in the pathogenesis of specific cardiovascular diseases. We cordially encourage you to contribute to this task.

Dr. Olga Kruszelnicka
Guest Editor

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

chemokines
cytokines
leukocyte trafficking
leukocyte attracting
leukocyte-derived cytokines
nitric oxide
prostacyclin
adhesion molecules
endothelium

Published Papers (3 papers)

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Research

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12 pages, 1466 KiB

Open AccessArticle

Coronary Slow-Flow Phenomenon in Takotsubo Syndrome: The Prevalence, Clinical Determinants, and Long-Term Prognostic Impact

by Konrad Stępień, Karol Nowak, Aleksandra Karcińska, Grzegorz Horosin, Alicia del Carmen Yika, Julia Lenart, Anna Górowska, Sylwia Iwańczyk, Mateusz Podolec, Aleksander Siniarski, Jadwiga Nessler and Jarosław Zalewski

Int. J. Mol. Sci. 2024, 25(2), 1297; https://doi.org/10.3390/ijms25021297 - 20 Jan 2024

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Abstract

Patients with takotsubo syndrome (TTS) may present coronary slow flow (CSF) in angiography performed in the acute myocardial infarction (MI). However, the detailed clinical relevance and its long-term impact remain poorly understood. Among 7771 MI patients hospitalized between 2012 and 2019, TTS was identified in 82 (1.1%) subjects. The epicardial blood flow was assessed with thrombolysis in myocardial infarction (TIMI) scale and corrected TIMI frame count (TFC), whereas myocardial perfusion with TIMI myocardial perfusion grade (TMPG). CSF was defined as TIMI-2 or corrected TFC > 27 frames in at least one epicardial vessel. CSF was identified in 33 (40.2%) TTS patients. In the CSF-TTS versus normal-flow-TTS group, lower values of left ventricular ejection fraction on admission (33.5 (25–40) vs. 40 (35–45)%, p = 0.019), more frequent midventricular TTS (27.3 vs. 8.2%, p = 0.020) and the coexistence of both physical and emotional triggers (9.1 vs. 0%, p = 0.032) were noted. Within a median observation of 55 months, higher all-cause mortality was found in CSF-TTS compared with normal-flow TTS (30.3 vs. 10.2%, p = 0.024). CSF was identified as an independent predictor of long-term mortality (hazard ratio 10.09, 95% confidence interval 2.12–48.00, p = 0.004). CSF identified in two-fifths of TTS patients was associated with unfavorable long-term outcomes. Full article

(This article belongs to the Special Issue Endothelial Dysfunction and Cardiovascular Diseases)

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15 pages, 2905 KiB

Open AccessArticle

Endothelial Cell Apoptosis but Not Necrosis Is Inhibited by Ischemic Preconditioning

by Jarosław Zalewski, Marta Szajna, Konrad Stępień, Karol Nowak, Aleksandra Karcińska, Alicia del Carmen Yika, Kornelia Krawczyk, Krzysztof Karwat, Magdalena Zalewska and Piotr Pierzchalski

Int. J. Mol. Sci. 2024, 25(2), 1238; https://doi.org/10.3390/ijms25021238 - 19 Jan 2024

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Abstract

This study aimed to assess the influence of ischemic preconditioning (IP) on hypoxia/reoxygenation (HR)-induced endothelial cell (EC) death. Human umbilical vein endothelial cells (HUVECs) were subjected to 2 or 6 h hypoxia with subsequent reoxygenation. IP was induced by 20 min of hypoxia followed by 20 min of reoxygenation. Necrosis was assessed by the release of lactate dehydrogenase (LDH) and apoptosis by double staining with propidium iodide/annexin V (PI/AV), using TUNEL test, and Bcl-2 and Bax gene expression measured using RT-PCR. In PI/AV staining, after 24 h of reoxygenation, 30–33% of EC were necrotic and 16–21% were apoptotic. In comparison to HR cells, IP reduced membrane apoptosis after 24 h of reoxygenation by 50% but did not influence EC necrosis. Nuclear EC apoptosis affected about 15–17% of EC after 24 h of reoxygenation and was reduced with IP by 55–60%. IP was associated with a significantly higher Bcl-2/Bax ratio, at 8 h 2–4 times and at 24 h 2–3 times as compared to HR. Longer hypoxia was associated with lower values of Bcl-2/Bax ratio in EC subjected to HR or IP. IP delays, without reducing, the extent of HR-induced EC necrosis but significantly inhibits their multi-level evaluated apoptosis. Full article

(This article belongs to the Special Issue Endothelial Dysfunction and Cardiovascular Diseases)

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Review

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20 pages, 900 KiB

Open AccessReview

Unveiling the Role of Endothelial Dysfunction: A Possible Key to Enhancing Catheter Ablation Success in Atrial Fibrillation

by George E. Zakynthinos, Vasiliki Tsolaki, Evangelos Oikonomou, Panteleimon Pantelidis, Ioannis Gialamas, Konstantinos Kalogeras, Epaminondas Zakynthinos, Manolis Vavuranakis and Gerasimos Siasos

Int. J. Mol. Sci. 2024, 25(4), 2317; https://doi.org/10.3390/ijms25042317 - 15 Feb 2024

Viewed by 544

Abstract

Atrial fibrillation, a prevalent type of arrhythmia, is increasingly contributing to the economic burden on healthcare systems. The development of innovative treatments, notably catheter ablation, has demonstrated both impressive and promising outcomes. However, these treatments have not yet fully replaced pharmaceutical approaches, primarily due to the relatively high incidence of atrial fibrillation recurrence post-procedure. Recent insights into endothelial dysfunction have shed light on its role in both the onset and progression of atrial fibrillation. This emerging understanding suggests that endothelial function might significantly influence the effectiveness of catheter ablation. Consequently, a deeper exploration into endothelial dynamics could potentially elevate the status of catheter ablation, positioning it as a primary treatment option for atrial fibrillation. Full article

(This article belongs to the Special Issue Endothelial Dysfunction and Cardiovascular Diseases)

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