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Endothelial Function and Cardiovascular Disease: Molecular Advances and Challenges
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Endothelial Function and Cardiovascular Disease: Molecular Advances and Challenges

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 (31 July 2026) | Viewed by 7019

Editor

Dr. Elena Grossini

E-Mail Website
Guest Editor
Department of Translational Medicine, University Eastern Piedmont, 28100 Novara, Italy
Interests: oxidative stress; cardiac function; mitochondrial function; aging; nitric oxide; physiology; NAFLD; microvesicles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The keeping endothelial function plays a central role for the regulation of physiologic processes related to the cardiovascular system. In general, endothelial activation, inflammation, and oxidative stress may represent the starting points leading to later events, like endothelial-to-mesenchymal transition and endothelial apoptosis, which result in the loss of endothelial function and the genesis of various cardiovascular diseases. This phenomenon has a multifactorial nature, being influenced by genetics and aging, as well as lifestyle.

Understanding the dynamic interplay between the above causes and traditional risks factors is crucial for the prevention of cardiovascular diseases and to tailor therapeutic interventions focused on the treatment of the different pathologies by targeting the underlying mechanism(s).

Speaking about molecular advances, pathways related to endothelial senescence, such as those involving sirtuins, klotho, and nuclear factor-E2-related factor 2 (NRF2), could represent interesting and innovative therapeutic targets to treat or prevent cardiovascular aging and age-related vascular pathologies. Also, endothelium-derived vesicles could act both as biomarkers and contributors to the onset and progression of cardiovascular diseases and represent challenges.

The aim of this Special Issue is to collect information about innovative aspects related to the regulation of endothelial functions and about their role in the genesis of cardiovascular diseases. Thanks to the knowledge of molecular advances in this field, it could be possible to gain a comprehensive understanding of endothelial dysfunctions and to develop strategies to mitigate their impact on cardiovascular diseases’ onset and progression.

Dr. Elena Grossini
Guest Editor

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-anonymized 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.

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Keywords

  • endothelium
  • heart
  • protection
  • therapeutic strategies
  • vascular system
  • vesicles

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Published Papers (5 papers)

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Research

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15 pages, 608 KB  
Article
Assessment of Blood Endothelial Cell Biomarkers in Women and Men with Abnormal Body Mass and Paroxysmal Atrial Fibrillation Based on CHA2DS2-VASC Score: A Retrospective Study
by Wiesław Sikora, Dominika Kanikowska, Jan Budzianowski, Edyta Kawka, Rafał Rutkowski and Katarzyna Korybalska
Int. J. Mol. Sci. 2025, 26(8), 3627; https://doi.org/10.3390/ijms26083627 - 11 Apr 2025
Cited by 3 | Viewed by 1339
Abstract
Endothelial dysfunction (ED) promotes and maintains atrial fibrillation (AF). Using a CHA2DS2-VASc score in women and men with paroxysmal AF, we aimed to determine which patients’ ED would be more pronounced. We recruited 47 females and 48 males (mean BMI 31 kg/m2 [...] Read more.
Endothelial dysfunction (ED) promotes and maintains atrial fibrillation (AF). Using a CHA2DS2-VASc score in women and men with paroxysmal AF, we aimed to determine which patients’ ED would be more pronounced. We recruited 47 females and 48 males (mean BMI 31 kg/m2 and 30 kg/m2, respectively) with paroxysmal AF and abnormal body mass and divided them into those with low (F < 3; M < 2) and high (F ≥ 3; M ≥ 2) CHA2DS2-VASC score. The blood samples were taken before AF ablation. Using Elisa tests, we measured tissue plasminogen activator (t-PA), plasminogen activator inhibitor 1 (PAI-1), vascular cell adhesion molecule 1 (sVCAM-1), intercellular adhesion molecule (sICAM-1), von Willebrand factor (vWF), and thrombomodulin (sTM). ED was more pronounced in females, expressed by higher endothelial cell marker concentrations: sVCAM-1 and sTM in low scores and sICAM-1 in high scores, CHA2DS2-VASc. Females were characterized by postmenopausal status, higher risk of thrombosis, lower GFR, and more frequent treatment with antiarrhythmic drugs. In contrast, males have only higher suppression of tumorigenicity 2 (ST2). In conclusion, women with paroxysmal AF exhibited more pronounced ED compared to men, regardless of their CHA2DS2-VASc scores. The soluble pro-inflammatory adhesion molecules and thrombomodulin emerge as the most sensitive biomarkers of ED elevated in females. Full article
(This article belongs to the Special Issue Endothelial Function and Cardiovascular Disease: Molecular Advances and Challenges)
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25 pages, 5834 KB  
Article
Characterization of Circulating Vesicles of Complicated and Uncomplicated Systemic Sclerosis Patients and Their Role in Vascular Dysfunction
by Elena Grossini, Mattia Bellan, Sakthipriyan Venkatesan, Mohammad Mostafa Ola Pour, Marco Mennuni, Domenico D’Amario, Stefania Bruno, Daniela Ferrante, Daniela Capello, Pier Paolo Sainaghi, Mario Pirisi and Giuseppe Patti
Int. J. Mol. Sci. 2025, 26(6), 2380; https://doi.org/10.3390/ijms26062380 - 7 Mar 2025
Cited by 6 | Viewed by 1537
Abstract
Extracellular vesicles (EVs) could be involved in the onset of systemic sclerosis (SSc) through the modulation of vascular function. Anyway, available data are contradictory, and further investigation would be necessary to clarify this aspect. Here, we characterized circulating EVs isolated from SSc patients [...] Read more.
Extracellular vesicles (EVs) could be involved in the onset of systemic sclerosis (SSc) through the modulation of vascular function. Anyway, available data are contradictory, and further investigation would be necessary to clarify this aspect. Here, we characterized circulating EVs isolated from SSc patients and evaluated their effects on human vascular endothelial cells (HUVECs) and smooth muscle cells. In EVs from 13 complicated and 27 uncomplicated SSc patients and five healthy controls (HCs), we analyzed the size, concentration, and surface marker expression. In addition, EVs were used to stimulate HUVECs, and we evaluated cell viability, mitochondrial membrane potential, and nitric oxide (NO) and mitochondrial reactive oxygen species (MitoROS) release. In smooth muscle cells, the effects of EVs on calcium movement were examined. The results showed that the EVs of SSc patients expressed markers of T-lymphocyte/platelet/endothelial cell origin and were larger and more concentrated than those from HCs. In addition, the EVs of SSc patients reduced cell viability and mitochondrial membrane potential and increased NO and MitoROS release in HUVECs and intracellular calcium in smooth muscle cells. In conclusion, we found a specific pattern for EVs isolated from SSc patients, which could have a pathogenic role through direct actions on endothelial and smooth muscle cells. Full article
(This article belongs to the Special Issue Endothelial Function and Cardiovascular Disease: Molecular Advances and Challenges)
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Review

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28 pages, 3984 KB  
Review
Shock Induced Endotheliopathy and High Trauma Mortality—Fight-or-Flight Response Revisited
by Nathan Weinstein, John B. Holcomb and Pär I. Johansson
Int. J. Mol. Sci. 2026, 27(16), 7210; https://doi.org/10.3390/ijms27167210 - 12 Aug 2026
Viewed by 228
Abstract
Trauma with hemorrhagic shock causes about 2.3 million deaths yearly worldwide. Improved hemostatic management has shifted the relative distribution of mortality, leaving multiorgan failure (MOF) as a leading cause of death. Clinical observations suggest that the evolutionarily ancient and well-conserved sympathetic system and [...] Read more.
Trauma with hemorrhagic shock causes about 2.3 million deaths yearly worldwide. Improved hemostatic management has shifted the relative distribution of mortality, leaving multiorgan failure (MOF) as a leading cause of death. Clinical observations suggest that the evolutionarily ancient and well-conserved sympathetic system and the microvascular endothelium are involved, and the experimental evidence is reviewed here. The analyzed clinical studies, human endothelial cell (EC) culture, and animal model-based experiments delineate how excess catecholamine levels increase endothelial cell reactive oxygen species production, causing glycocalyx damage and thrombomodulin cleavage. This leads to a prothrombotic EC surface, resulting in coagulation activation and thrombus formation that leaves tissues prone to hypoxia. Excess catecholamines also increase endothelial barrier permeability, leading to fluid extravasation, elevated tissue pressure, and hypoxia. The reviewed experimental data support, but do not yet prove, dysregulated sympathetic activation’s critical contribution to the development of shock-induced endotheliopathy prone to tissue hypoxia and, ultimately, death from coagulopathy, loss of immune competence, and MOF, as observed clinically in shocked trauma patients. Due to the physiological differences between humans and model organisms, and EC culture growth conditions, some molecular mechanisms require further investigation through clinical studies and targeted experiments. Full article
(This article belongs to the Special Issue Endothelial Function and Cardiovascular Disease: Molecular Advances and Challenges)
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18 pages, 1744 KB  
Review
Hyperglycemia-Induced Endothelial Dysfunction: From Classical Pathogenetic Mechanisms to Emerging Insights into ACE2 Protective Action
by Giada Lodi, Domenico Sergi, Anna Dipinto, Francesca Bompan, Paola Secchiero, Rebecca Voltan and Arianna Romani
Int. J. Mol. Sci. 2026, 27(6), 2660; https://doi.org/10.3390/ijms27062660 - 14 Mar 2026
Cited by 5 | Viewed by 2451
Abstract
Diabetes is a pivotal risk factor for cardiovascular disease as well as microvascular complications, including retinopathy and nephropathy. Chronic hyperglycemia is a key player in linking diabetes with endothelial dysfunction which, in turn, contributes to cardiovascular disease. Indeed, hyperglycemia acts as a trigger [...] Read more.
Diabetes is a pivotal risk factor for cardiovascular disease as well as microvascular complications, including retinopathy and nephropathy. Chronic hyperglycemia is a key player in linking diabetes with endothelial dysfunction which, in turn, contributes to cardiovascular disease. Indeed, hyperglycemia acts as a trigger for endothelial dysfunction, promoting a shift in the endothelium from a protective, anti-inflammatory state to a dysfunctional, injury-prone phenotype. A hyperglycemic environment triggers several pathogenetic mechanisms, including alterations in bioenergetics, production of advanced glycation end products, oxidative stress and mitochondrial dysfunction, all contributing to endothelial dysfunction. The activation of these pathophysiological mechanisms by hyperglycemia culminates in reduced nitric oxide production, as well as the induction of oxidative stress and inflammation, all of which are pivotal in impairing endothelial homeostasis and promoting cellular damage. Besides these classical mechanisms, there is growing attention on novel pathogenetic factors linking diabetic hyperglycemia with endothelial dysfunction, such as the ACE2 protein. The latter is emergeing for its potential to counter hyperglycemia-induced cellular damage through its vasoprotective and anti-inflammatory actions, making it a promising therapeutic target for tackling endothelial dysfunction. This review provides an overview of classical as well as emerging mechanisms underpinning the deleterious effects of diabetic hyperglycemia on endothelial dysfunction. In turn, understanding the molecular interconnections between hyperglycemia and endothelial dysfunction is crucial for developing novel strategies to restore endothelial homeostasis and mitigate diabetic vascular complications. Full article
(This article belongs to the Special Issue Endothelial Function and Cardiovascular Disease: Molecular Advances and Challenges)
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Other

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7 pages, 201 KB  
Opinion
Rare Models: Use of a Novel Translational Model for Diffuse Alveolar Haemorrhage
by Karan R. Chadda, Savithri Sathivelu, Susan K. Armstrong, Charlotte Edling and Kamalan Jeevaratnam
Int. J. Mol. Sci. 2026, 27(10), 4157; https://doi.org/10.3390/ijms27104157 - 7 May 2026
Viewed by 506
Abstract
Diffuse alveolar haemorrhage (DAH) is rare but associated with high morbidity and mortality. It is underpinned by mechanisms of endothelial dysfunction, inflammation, and vascular remodelling, yet its pathogenesis remains incompletely understood. Progress in translational research is currently limited by the absence of robust [...] Read more.
Diffuse alveolar haemorrhage (DAH) is rare but associated with high morbidity and mortality. It is underpinned by mechanisms of endothelial dysfunction, inflammation, and vascular remodelling, yet its pathogenesis remains incompletely understood. Progress in translational research is currently limited by the absence of robust animal models of this condition. Equine exercise-induced pulmonary haemorrhage (EIPH), a common and progressive disorder in racehorses, may represent a novel and underutilised translational model for studying DAH, which can be a complication of or associated with other cardiopulmonary conditions, such as pulmonary arterial hypertension (PAH). EIPH occurs spontaneously in up to 95% of thoroughbreds after repeated strenuous exercise and is characterised by haemorrhage into the alveoli, capillary stress failure, inflammatory infiltration, and subsequent parenchymal remodelling. These processes closely parallel the vascular injury and immune activation observed in DAH. Horses further offer distinct advantages as models for human respiratory disease, including large lung size, long lifespan, and comparable pulmonary architecture. The regional distribution of haemorrhage in equine lungs additionally enables within-animal control studies. By leveraging the mechanistic overlaps between equine and human pulmonary pathology, EIPH provides a unique opportunity for biomarker discovery, mechanistic insight, and therapeutic testing in pulmonary vascular disease. Full article
(This article belongs to the Special Issue Endothelial Function and Cardiovascular Disease: Molecular Advances and Challenges)
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