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Biomedicines
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Role of Endothelial Cells in Cardiovascular Disease
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Role of Endothelial Cells in Cardiovascular Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 12695

Special Issue Editors

Dr. Lorenzo Falsetti

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Guest Editor
Department of Emergency Medicine, Internal and Sub-Intensive Medicine, Azienda Ospedaliero-Universitaria "Ospedali Riuniti", 60166 Ancona, Italy
Interests: endothelial cells; atherosclerosis; endothelial progenitor cells; deep vein thrombosis; pulmonary embolism; cardiovascular regenerative medicine; sepsis and septic shock
Special Issues, Collections and Topics in MDPI journals
Dr. Vincenzo Zaccone

E-Mail Website
Guest Editor
Department of Emergency Medicine, Internal and Sub-Intensive Medicine, Azienda Ospedaliero-Universitaria "Ospedali Riuniti", 60166 Ancona, Italy
Interests: endothelial cells; atherosclerosis; endothelial progenitor cells; deep vein thrombosis; pulmonary embolism; cardiovascular regenerative medicine; sepsis and septic shock
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endothelial cells’ function plays a pivotal role in cardiovascular system homeostasis through the regulation of several blood vessels’ functions such as vasodilation, inflammation and thrombosis. Cardiovascular diseases represent a leading cause of mortality and morbidity, and endothelial dysfunction contributes to their pathogenesis. Thus, increasing our knowledge regarding endothelial cells’ pathophysiology in the setting of cardiovascular diseases is strongly advised in order to prevent and treat the most important cardiac and vascular pathologies such as hypertension, diabetes, intimal hyperplasia, venous and arterial thrombosis, and heart diseases.

This Special Issue welcomes basic and clinical research, covering original articles and reviews on:

  • Endothelial cells’ physiology and pathophysiology;
  • Endothelial cells’ role in the pathogenesis of acute and chronic cardiovascular diseases;
  • The role of acute and chronic systemic diseases in the genesis of endothelial dysfunction;
  • New pharmacological approaches for endothelial dysfunction;
  • Endothelial progenitor cells and cardiovascular regenerative medicine.

Dr. Lorenzo Falsetti
Dr. Vincenzo Zaccone
Guest Editors

Manuscript Submission Information

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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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

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Published Papers (6 papers)

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Research

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16 pages, 2434 KiB  
Article
Prolonged Door-to-Balloon Time Leads to Endothelial Glycocalyx Damage and Endothelial Dysfunction in Patients with ST-Elevation Myocardial Infarction
by Carl Vahldieck, Benedikt Fels, Samuel Löning, Laura Nickel, Joachim Weil and Kristina Kusche-Vihrog
Biomedicines 2023, 11(11), 2924; https://doi.org/10.3390/biomedicines11112924 - 29 Oct 2023
Cited by 1 | Viewed by 1333
Abstract
Damage to the endothelial glycocalyx (eGC) has been reported during acute ischemic events like ST-elevation myocardial infarction (STEMI). In STEMI, a door-to-balloon time (D2B) of <60 min was shown to reduce mortality and nonfatal complications. Here, we hypothesize that eGC condition is associated [...] Read more.
Damage to the endothelial glycocalyx (eGC) has been reported during acute ischemic events like ST-elevation myocardial infarction (STEMI). In STEMI, a door-to-balloon time (D2B) of <60 min was shown to reduce mortality and nonfatal complications. Here, we hypothesize that eGC condition is associated with D2B duration and endothelial function during STEMI. One hundred and twenty-six individuals were analyzed in this study (STEMI patients vs. age-/sex-matched healthy volunteers). After stimulating endothelial cells with patient/control sera, the eGC’s nanomechanical properties (i.e., height/stiffness) were analyzed using the atomic force microscopy-based nanoindentation technique. eGC components were determined via ELISA, and measurements of nitric oxide levels (NO) were based on chemiluminescence. eGC height/stiffness (both p < 0.001), as well as NO concentration (p < 0.001), were reduced during STEMI. Notably, the D2B had a strong impact on the endothelial condition: a D2B > 60 min led to significantly higher serum concentrations of eGC components (syndecan-1: p < 0.001/heparan sulfate: p < 0.001/hyaluronic acid: p < 0.0001). A D2B > 60 min led to the pronounced loss of eGC height/stiffness (both, p < 0.001) with reduced NO concentrations (p < 0.01), activated the complement system (p < 0.001), and prolonged the hospital stay (p < 0.01). An increased D2B led to severe eGC shedding, with endothelial dysfunction in a temporal context. eGC components and pro-inflammatory mediators correlated with a prolonged D2B, indicating a time-dependent immune reaction during STEMI, with a decreased NO concentration. Thus, D2B is a crucial factor for eGC damage during STEMI. Clinical evaluation of the eGC condition might serve as an important predictor for the endothelial function of STEMI patients in the future. Full article
(This article belongs to the Special Issue Role of Endothelial Cells in Cardiovascular Disease)
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15 pages, 5927 KiB  
Article
GSDME in Endothelial Cells: Inducing Vascular Inflammation and Atherosclerosis via Mitochondrial Damage and STING Pathway Activation
by Shiyao Xie, Enyong Su, Xiaoyue Song, Junqiang Xue, Peng Yu, Baoli Zhang, Ming Liu and Hong Jiang
Biomedicines 2023, 11(9), 2579; https://doi.org/10.3390/biomedicines11092579 - 20 Sep 2023
Cited by 1 | Viewed by 2068
Abstract
The initiation of atherosclerotic plaque is characterized by endothelial cell inflammation. In light of gasdermin E’s (GSDME) role in pyroptosis and inflammation, this study elucidates its function in atherosclerosis onset. Employing Gsdme- and apolipoprotein E-deficient (Gsdme−/−/ApoE−/−) and ApoE [...] Read more.
The initiation of atherosclerotic plaque is characterized by endothelial cell inflammation. In light of gasdermin E’s (GSDME) role in pyroptosis and inflammation, this study elucidates its function in atherosclerosis onset. Employing Gsdme- and apolipoprotein E-deficient (Gsdme−/−/ApoE−/−) and ApoE−/− mice, an atherosclerosis model was created on a Western diet (WD). In vitro examinations with human umbilical vein endothelial cells (HUVECs) included oxidized low-density lipoprotein (ox-LDL) exposure. To explore the downstream mechanisms linked to GSDME, we utilized an agonist targeting the stimulator of the interferon genes (STING) pathway. The results showed significant GSDME activation in ApoE−/− mice arterial tissues, corresponding with atherogenesis. Gsdme−/−/ApoE−/− mice displayed fewer plaques and decreased vascular inflammation. Meanwhile, GSDME’s presence was confirmed in endothelial cells. GSDME inhibition reduced the endothelial inflammation induced by ox-LDL. GSDME was linked to mitochondrial damage in endothelial cells, leading to an increase in cytoplasmic double-stranded DNA (dsDNA). Notably, STING activation partially offset the effects of GSDME inhibition in both in vivo and in vitro settings. Our findings underscore the pivotal role of GSDME in endothelial cells during atherogenesis and vascular inflammation, highlighting its influence on mitochondrial damage and the STING pathway, suggesting a potential therapeutic target for vascular pathologies. Full article
(This article belongs to the Special Issue Role of Endothelial Cells in Cardiovascular Disease)
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15 pages, 3548 KiB  
Article
Human Lactoferrin Synergizes with Etoposide to Inhibit Lung Adenocarcinoma Cell Growth While Attenuating Etoposide-Mediated Cytotoxicity of Human Endothelial Cells
by Paulina Olszewska, Barbara Pazdrak and Marian L. Kruzel
Biomedicines 2022, 10(10), 2429; https://doi.org/10.3390/biomedicines10102429 - 28 Sep 2022
Cited by 2 | Viewed by 1905
Abstract
Lung cancer continues to be the deadliest cancer worldwide. A new strategy of combining chemotherapeutics with naturally occurring anticancer compounds, such as lactoferrin, might improve the efficacy and toxicity of current chemotherapy. The aim of this study was to evaluate the effect of [...] Read more.
Lung cancer continues to be the deadliest cancer worldwide. A new strategy of combining chemotherapeutics with naturally occurring anticancer compounds, such as lactoferrin, might improve the efficacy and toxicity of current chemotherapy. The aim of this study was to evaluate the effect of recombinant human lactoferrin (rhLf) in combination with etoposide on anticancer activity in human lung adenocarcinoma cells. In addition, we examined the impact of rhLf on etoposide-induced cytotoxicity of human endothelial cells. We found that treatment of A549 cells with a combination of etoposide and rhLf resulted in significantly greater inhibition of cancer cell growth as compared to etoposide alone. The combination repressed cancer cell growth by cell cycle arrest in the G2/M phase and induction of apoptosis. In contrast to cancer cells, rhLf did not affect endothelial cell viability. Importantly, rhLf significantly diminished the etoposide-induced cytotoxicity of endothelial cells. Analysis of the type of drug interaction based on combination index value showed that rhLf synergized with etoposide to induce anticancer activity. The calculated dose reduction index indicated that the combination treatment reduced a 10-fold of etoposide dose to achieve the same anticancer effect. Our data demonstrate that rhLf enhanced the anticancer activity of etoposide and diminished etoposide-induced cytotoxic effect in endothelial cells. Full article
(This article belongs to the Special Issue Role of Endothelial Cells in Cardiovascular Disease)
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Review

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20 pages, 1674 KiB  
Review
Decoding Pulmonary Embolism: Pathophysiology, Diagnosis, and Treatment
by Miriam Peracaula, Laura Sebastian, Iria Francisco, Marc Bonnin Vilaplana, Diego A. Rodríguez-Chiaradía and Olga Tura-Ceide
Biomedicines 2024, 12(9), 1936; https://doi.org/10.3390/biomedicines12091936 - 23 Aug 2024
Viewed by 1954
Abstract
Pulmonary Embolism (PE) is a life-threatening condition initiated by the presence of blood clots in the pulmonary arteries, leading to severe morbidity and mortality. Underlying mechanisms involve endothelial dysfunction, including impaired blood flow regulation, a pro-thrombotic state, inflammation, heightened oxidative stress, and altered [...] Read more.
Pulmonary Embolism (PE) is a life-threatening condition initiated by the presence of blood clots in the pulmonary arteries, leading to severe morbidity and mortality. Underlying mechanisms involve endothelial dysfunction, including impaired blood flow regulation, a pro-thrombotic state, inflammation, heightened oxidative stress, and altered vascular remodeling. These mechanisms contribute to vascular diseases stemming from PE, such as recurrent thromboembolism, chronic thromboembolic pulmonary hypertension, post-thrombotic syndrome, right heart failure, and cardiogenic shock. Detailing key risk factors and utilizing hemodynamic stability-based categorization, the review aims for precise risk stratification by applying established diagnostic tools and scoring systems. This article explores both conventional and emerging biomarkers as potential diagnostic tools. Additionally, by synthesizing existing knowledge, it provides a comprehensive outlook of the current enhanced PE management and preventive strategies. The conclusion underscores the need for future research to improve diagnostic accuracy and therapeutic effectiveness in PE. Full article
(This article belongs to the Special Issue Role of Endothelial Cells in Cardiovascular Disease)
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15 pages, 1558 KiB  
Review
Wnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications
by Rizwana Afroz and Julie E. Goodwin
Biomedicines 2024, 12(2), 276; https://doi.org/10.3390/biomedicines12020276 - 25 Jan 2024
Viewed by 1782
Abstract
Atherosclerosis is a vascular disease in which inflammation plays a pivotal role. Receptor-mediated signaling pathways regulate vascular inflammation and the pathophysiology of atherosclerosis. Emerging evidence has revealed the role of the Wnt pathway in atherosclerosis progression. The Wnt pathway influences almost all stages [...] Read more.
Atherosclerosis is a vascular disease in which inflammation plays a pivotal role. Receptor-mediated signaling pathways regulate vascular inflammation and the pathophysiology of atherosclerosis. Emerging evidence has revealed the role of the Wnt pathway in atherosclerosis progression. The Wnt pathway influences almost all stages of atherosclerosis progression, including endothelial dysfunction, monocyte infiltration, smooth muscle cell proliferation and migration, and plaque formation. Targeting the Wnt pathway to treat atherosclerosis represents a promising therapeutic approach that remains understudied. Blocking Wnt signaling utilizing small molecule inhibitors, recombinant proteins, and/or neutralizing antibodies ameliorates atherosclerosis in preclinical models. The Wnt pathway can be potentially manipulated through targeting Wnt ligands, receptors, co-receptors, and downstream signaling molecules. However, there are challenges associated with developing a real world therapeutic compound that targets the Wnt pathway. This review focuses on the role of Wnt signaling in atherosclerosis development, and the rationale for targeting this pathway for the treatment of atherosclerosis. Full article
(This article belongs to the Special Issue Role of Endothelial Cells in Cardiovascular Disease)
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18 pages, 930 KiB  
Review
Role of Endothelium in Cardiovascular Sequelae of Long COVID
by Luca Santoro, Vincenzo Zaccone, Lorenzo Falsetti, Vittorio Ruggieri, Martina Danese, Chiara Miro, Angela Di Giorgio, Antonio Nesci, Alessia D’Alessandro, Gianluca Moroncini and Angelo Santoliquido
Biomedicines 2023, 11(8), 2239; https://doi.org/10.3390/biomedicines11082239 - 9 Aug 2023
Cited by 16 | Viewed by 2690
Abstract
The global action against coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2 infection, shed light on endothelial dysfunction. Although SARS-CoV-2 primarily affects the pulmonary system, multiple studies have documented pan-vascular involvement in COVID-19. The virus is able to penetrate the endothelial barrier, damaging it [...] Read more.
The global action against coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2 infection, shed light on endothelial dysfunction. Although SARS-CoV-2 primarily affects the pulmonary system, multiple studies have documented pan-vascular involvement in COVID-19. The virus is able to penetrate the endothelial barrier, damaging it directly or indirectly and causing endotheliitis and multi-organ injury. Several mechanisms cooperate to development of endothelial dysfunction, including endothelial cell injury and pyroptosis, hyperinflammation and cytokine storm syndrome, oxidative stress and reduced nitric oxide bioavailability, glycocalyx disruption, hypercoagulability, and thrombosis. After acute-phase infection, some patients reported signs and symptoms of a systemic disorder known as long COVID, in which a broad range of cardiovascular (CV) disorders emerged. To date, the exact pathophysiology of long COVID remains unclear: in addition to the persistence of acute-phase infection mechanisms, specific pathways of CV damage have been postulated, such as persistent viral reservoirs in the heart or an autoimmune response to cardiac antigens through molecular mimicry. The aim of this review is to provide an overview of the main molecular patterns of enduring endothelial activation following SARS-CoV-2 infection and to offer the latest summary of CV complications in long COVID. Full article
(This article belongs to the Special Issue Role of Endothelial Cells in Cardiovascular Disease)
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