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Special Issue "10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction"

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 31 October 2023 | Viewed by 19703

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Dr. Manfredi Tesauro

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Guest Editor

U.O.C. of Internal Medicine—Center of Hypertension and Nephrology Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy
Interests: endothelial dysfunction; obesity; insulin resistance; diabetic nephropathy; metabolic syndrome; adipokines
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Carmine Cardillo

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Guest Editor

Department of Translational Medicine and Surgery, Catholic University, Rome, Italy
Interests: obesity; metabolic syndrome; endothelial function; hypertension

Special Issue Information

Dear Colleagues,

The year 2022 marks the 10th anniversary of Biomedicines, a peer-reviewed open access journal in the biomedical field. Thus far, Biomedicines has published more than 2700 papers from more than 17,000 authors. We appreciate each author, reviewer, and academic editor whose support has brought us to where we are today. To celebrate this significant milestone, we aim to publish a Special Issue entitled “10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction".

Endothelial dysfunction is an early marker of atherosclerosis. Under normal conditions, vascular endothelium maintains blood vessels and keeps them in good shape though synthesis and release of several vasodilatory, anti-inflammatory, and antithombotic substances. Principal among these substances is nitric oxide (NO), which plays a central role in the maintenance of vascular homeostasis. When endothelial dysfunction is induced by pathological stresses, such as hyperlipidemia, hypertension, and hyperglycemia, among others, NO production is impaired and the protective effect of endothelium is disrupted, with consequent vasoconstriction and “activation” of endothelial cells that trigger a cascade of events, resulting in the formation of the atherosclerotic lesion.

Changes in adipose tissue related to obesity result in derangement in the main vascular homeostatic mechanisms, the NO pathway, and the endothelin-1 (ET-1) system, thereby leading to a vasoconstrictor and proatherogenic profile. Derangement of insulin signaling seems to play a central role in the pathophysiology of vascular dysfunction associated with obesity and metabolic syndrome; moreover, the vascular alterations associated with insulin resistance and obesity do not seem to be limited to the endothelium, but also involve other layers of the vessel wall, such as vascular smooth muscle and adventitial/perivascular fat. Perivascular adipose tissue (PVAT) is a potential source of the mediators that lead to obesity-related vascular damage, and conformational changes in perivascular fat have been shown to associate with a loss of anticontractile properties, likely due to inflammatory, vasoconstrictor, and oxidative mechanisms.

For this Special Issue, we are seeking research articles that will improve our knowledge on these topics. Both original research and review articles are welcome.

Prof. Dr. Manfredi Tesauro
Prof. Dr. Carmine Cardillo
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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

endothelial dysfunction
atherosclerosis
nitric oxide (NO)
hyperlipidemia
hypertension
hyperglycemia
vasodilation
perivascular adipose tissue (PVAT)
insulin resistance

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Biomedicines: 10th Anniversary in Biomedicines (31 articles)

Published Papers (11 papers)

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Research

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Open AccessArticle

Endothelial Function and Hypoxic–Hyperoxic Preconditioning in Coronary Surgery with a Cardiopulmonary Bypass: Randomized Clinical Trial

Andrey G. Yavorovskiy

and

Andrey I. Yaroshetskiy

Biomedicines 2023, 11(4), 1044; https://doi.org/10.3390/biomedicines11041044 - 28 Mar 2023

Viewed by 521

Abstract

A hypoxic–hyperoxic preconditioning (HHP) may be associated with cardioprotection by reducing endothelial damage and a beneficial effect on postoperative outcome in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Patients (n = 120) were randomly assigned to an HHP and a control group. A safe, inhaled oxygen fraction for the hypoxic preconditioning phase (10–14% oxygen for 10 min) was determined by measuring the anaerobic threshold. At the hyperoxic phase, a 75–80% oxygen fraction was used for 30 min. The cumulative frequency of postoperative complications was 14 (23.3%) in the HHP vs. 23 (41.1%), p = 0.041. The nitrate decreased after surgery by up to 20% in the HHP group and up to 38% in the control group. Endothelin-1 and nitric oxide metabolites were stable in HHP but remained low for more than 24 h in the control group. The endothelial damage markers appeared to be predictors of postoperative complications. The HHP with individual parameters based on the anaerobic threshold is a safe procedure, and it can reduce the frequency of postoperative complications. The endothelial damage markers appeared to be predictors of postoperative complications. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessArticle

The Long-Term Effects of Prenatal Hypoxia on Coronary Artery Function of the Male and Female Offspring

Christy-Lynn M. Cooke

and

Sandra T. Davidge

Biomedicines 2022, 10(12), 3019; https://doi.org/10.3390/biomedicines10123019 - 23 Nov 2022

Viewed by 953

Abstract

Prenatal hypoxia predisposes the offspring to the development of cardiovascular (CV) dysfunction in adult life. Using a rat model, we assessed the effect of prenatal hypoxia on vasoconstrictive and vasodilative mechanisms in left anterior descending coronary arteries of 4- and 9.5-month-old offspring. Endothelium-dependent relaxation to methylcholine and vasoconstriction responses to endothelin-1 (ET-1) were assessed by wire myography. Prenatal hypoxia impaired endothelium-dependent vasodilation in 4- and 9.5-month-old offspring. Inhibition of nitric oxide (NO) synthase prevented coronary artery relaxation in all groups. Inhibition of prostaglandin H synthase (PGHS) improved relaxation in prenatally hypoxic males and tended to improve vasorelaxation in females, suggesting that impaired vasodilation was mediated via increased PGHS-dependent vasoconstriction. An enhanced contribution of endothelium-dependent hyperpolarization to coronary artery vasodilation was observed in prenatally hypoxic males and females. No changes in endothelial NO synthase (eNOS) and PGHS-1 expressions were observed, while PGHS-2 expression was decreased in only prenatally hypoxic males. At 4 months, ET-1 responses were similar between groups, while ET_B inhibition (with BQ788) tended to decrease ET-1-mediated responses in only prenatally hypoxic females. At 9.5 months, ET-1-mediated responses were decreased in only prenatally hypoxic females. Our data suggest that prenatal hypoxia has long-term similar effects on the mechanisms of impaired endothelium-dependent vasodilation in coronary arteries from adult male and female offspring; however, coronary artery contractile capacity is impaired only in prenatally hypoxic females. Understanding the mechanistic pathways involved in the programming of CV disease may allow for the development of therapeutic interventions. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessArticle

Circulating Serum Cystatin C as an Independent Risk Biomarker for Vascular Endothelial Dysfunction in Patients with COVID-19-Associated Multisystem Inflammatory Syndrome in Children (MIS-C): A Prospective Observational Study

and

Biomedicines 2022, 10(11), 2956; https://doi.org/10.3390/biomedicines10112956 - 17 Nov 2022

Viewed by 872

Abstract

Introduction: Multisystem inflammatory syndrome in children (MIS-C) is a new clinical entity that has emerged in the context of the COVID-19 pandemic. Despite the less severe course of the disease, varying degrees of cardiovascular events may occur in MIS-C; however, data on vascular changes occurring in MIS-C are still lacking. Endothelial dysfunction (ED) is thought to be one of the key risk factors contributing to MIS-C. Background: We conducted a prospective observational study. We investigated possible manifestations of cardiac and endothelial involvement in MIS-C after the treatment of the acute stage and potential predictive biomarkers in patients with MIS-C. Methods: Twenty-seven consecutive pediatric subjects (≥9 years), at least three months post-treated MIS-C of varying severity, in a stable condition, and twenty-three age- and sex-matched healthy individuals (HI), were enrolled. A combined non-invasive diagnostic approach was used to assess endothelial function as well as markers of organ damage using cardiac examination and measurement of the reactive hyperemia index (RHI), by recording the post- to pre-occlusion pulsatile volume changes and biomarkers related to ED and cardiac disease. Results: MIS-C patients exhibited a significantly lower RHI (indicative of more severe ED) than those in HI (1.32 vs. 1.80; p = 0.001). The cutoff of RHI ≤ 1.4 was independently associated with a higher cardiovascular risk. Age and biomarkers significantly correlated with RHI, while serum cystatin C (Cys C) levels were independently associated with a diminished RHI, suggesting Cys C as a surrogate marker of ED in MIS-C. Conclusions: Patients after MIS-C display evidence of ED, as shown by a diminished RHI and altered endothelial biomarkers. Cys C was identified as an independent indicator for the development of cardiovascular disease. The combination of these factors has the potential to better predict the cardiovascular consequences of MIS-C. Our study suggests that ED may be implicated in the pathophysiology of this disease. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessArticle

Metformin Prevents Endothelial Dysfunction in Endometriosis through Downregulation of ET-1 and Upregulation of eNOS

Ana Filipa Martins

Ana Catarina Neto

Adriana Raquel Rodrigues

Sandra Marisa Oliveira

Cláudia Sousa-Mendes

Adelino Leite-Moreira

Alexandra Maria Gouveia

Henrique Almeida

and

Delminda Neves

Biomedicines 2022, 10(11), 2782; https://doi.org/10.3390/biomedicines10112782 - 01 Nov 2022

Viewed by 1041

Abstract

This study aimed to evaluate if the treatment with metformin affects the morphologic structure, endothelial function, angiogenesis, inflammation and oxidation-responsive pathways in the heart of mice with surgically induced endometriosis. B6CBA/F1 mice (n = 37) were divided into four groups; Sham (S), Metformin (M), Endometriosis (E) and Metformin/Endometriosis (ME). The cross-sectional area of cardiomyocytes was assessed after Hematoxylin–Eosin staining and fibrosis after Picrosirius-Red staining. ET-1, nitric oxide synthases-iNOS and eNOS, and VEGF and VEGFR-2 were detected by immunofluorescence. Semi-quantification of ET-1, eNOS, VEGF, NF-kB, Ikβα and KEAP-1 was performed by Western blotting. MIR199a, MIR16-1, MIR18a, MIR20a, MIR155, MIR200a, MIR342, MIR24-1 and MIR320a were quantified by Real-Time qPCR. The interaction of endometriosis and metformin effects was assessed by a two-way ANOVA test. Compared with the other groups, M-treated mice presented a higher cross-sectional area of cardiomyocytes. Heart fibrosis increased with endometriosis. Treatment of endometriosis with metformin in the ME group downregulates ET-1 and upregulates eNOS expression comparatively with the E group. However, metformin failed to mitigate NF-kB expression significantly incremented by endometriosis. The expression of MIR199a, MIR16-1 and MIR18a decreased with endometriosis, whereas MIR20a showed an equivalent trend, altogether reducing cardioprotection. In summary, metformin diminished endometriosis-associated endothelial dysfunction but did not mitigate the increase in NF-kB expression and cardiac fibrosis in mice with endometriosis. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessEditor’s ChoiceArticle

Bronchial Asthma as a Cardiovascular Risk Factor: A Prospective Observational Study

and

Biomedicines 2022, 10(10), 2614; https://doi.org/10.3390/biomedicines10102614 - 18 Oct 2022

Cited by 1 | Viewed by 5858

Abstract

Introduction: Asthma as a chronic inflammatory disorder has been suggested as a risk factor for endothelial dysfunction (ED), but studies on the association between asthma and cardiovascular disease (CVD) risk are limited. Background: We assessed associations of ED with the severity of asthma, eosinophilic inflammation, lung function, and asthma control. Methods: 52 young asthmatics (median age of 25.22 years) and 45 healthy individuals were included. Demographic, clinical, and laboratory findings were recorded. We evaluated microvascular responsiveness by recording the reactive hyperemia index (RHI) indicating post-occlusive peripheral endothelium-dependent changes in vascular tone using the Itamar Medical EndoPAT2000. VCAM-1, ADMA, high-sensitive CRP (hsCRP), and E-selectin were measured. Results: Asthmatics had considerably lower RHI values (p < 0.001) with a dynamic decreasing trend by asthma severity and higher hsCRP levels (p < 0.001). A substantial increase in hsCRP and E-selectin with asthma severity (p < 0.05) was also observed. We confirmed a higher body mass index (BMI) in asthmatics (p < 0.001), especially in women and in severe asthma. Conclusions: We demonstrated the progression of CVD in asthmatics and the association of the ongoing deterioration of ED with the inflammatory severity, suggesting that the increased risk of CVD in young asthmatics is dependent on disease severity. The underlying mechanisms of risk factors for CVD and disease control require further study. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Review

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Open AccessReview

Immunological and Metabolic Causes of Infertility in Polycystic Ovary Syndrome

Aleksandra Maria Kicińska

Radoslaw B. Maksym

Magdalena A. Zabielska-Kaczorowska

Aneta Stachowska

and

Anna Babińska

Biomedicines 2023, 11(6), 1567; https://doi.org/10.3390/biomedicines11061567 - 28 May 2023

Viewed by 531

Abstract

Infertility has been recognized as a civilizational disease. One of the most common causes of infertility is polycystic ovary syndrome (PCOS). Closely interrelated immunometabolic mechanisms underlie the development of this complex syndrome and lead to infertility. The direct cause of infertility in PCOS is ovulation and implantation disorders caused by low-grade inflammation of ovarian tissue and endometrium which, in turn, result from immune and metabolic system disorders. The systemic immune response, in particular the inflammatory response, in conjunction with metabolic disorders, insulin resistance (IR), hyperadrenalism, insufficient secretion of progesterone, and oxidative stress lead not only to cardiovascular diseases, cancer, autoimmunity, and lipid metabolism disorders but also to infertility. Depending on the genetic and environmental conditions as well as certain cultural factors, some diseases may occur immediately, while others may become apparent years after an infertility diagnosis. Each of them alone can be a significant factor contributing to the development of PCOS and infertility. Further research will allow clinical management protocols to be established for PCOS patients experiencing infertility so that a targeted therapy approach can be applied to the factor underlying and driving the “vicious circle” alongside symptomatic treatment and ovulation stimulation. Hence, therapy of fertility for PCOS should be conducted by interdisciplinary teams of specialists as an in-depth understanding of the molecular relationships and clinical implications between the immunological and metabolic factors that trigger reproductive system disorders is necessary to restore the physiology and homeostasis of the body and, thus, fertility, among PCOS patients. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessReview

Erectile Dysfunction: Pharmacological Pathways with Understudied Potentials

Doaa R. Adam

and

Manal M. Alem

Biomedicines 2023, 11(1), 46; https://doi.org/10.3390/biomedicines11010046 - 25 Dec 2022

Cited by 1 | Viewed by 1620

Abstract

Erectile dysfunction (ED) is a public health concern worldwide. In the past, it was perceived as a phenomenon attributed to age advancement. However, more individuals are affected every year that do not fall under that age criterion. Epidemiological research revealed that this abnormality has an association with endothelial dysfunction connected to several cardiovascular (CV) risk factors. Currently, ED is interpreted as a clinical marker for future adverse events and not only as a present health issue that negatively affects the quality of life. The management of ED involves lifestyle modifications, therapeutic optimization for comorbid conditions, and pharmacological and psychosexual therapy. Phosphodiesterase type 5 (PDE5) inhibitors are the first-line pharmacological agents to be prescribed for such a condition. Nonetheless, other pharmacological pathways and agents remain underinvestigated or were investigated at some stage. This review aimed to present to future researchers interested in this field with some pharmacological agents that showed favorable effects on a limited number of studies on human subjects or experimental models. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessReview

Endothelial Progenitor Cells in Neurovascular Disorders—A Comprehensive Overview of the Current State of Knowledge

and

Biomedicines 2022, 10(10), 2616; https://doi.org/10.3390/biomedicines10102616 - 18 Oct 2022

Viewed by 1136

Abstract

Endothelial progenitor cells (EPCs) are a population of cells that circulate in the blood looking for areas of endothelial or vascular injury in order to repair them. Endothelial dysfunction is an important component of disorders with neurovascular involvement. Thus, the subject of involvement of EPCs in such conditions has been gaining increasing scientific interest in recent years. Overall, decreased levels of EPCs are associated with worse disease outcome. Moreover, their functionalities appear to decline with severity of disease. These findings inspired the application of EPCs as therapeutic targets and agents. So far, EPCs appear safe and promising based on the results of pre-clinical studies conducted on their use in the treatment of Alzheimer’s disease and ischemic stroke. In the case of the latter, human clinical trials have recently started to be performed in this subject and provided optimistic results thus far. Whereas in the case of migraine, existing findings pave the way for testing EPCs in in vitro studies. This review aims to thoroughly summarize current knowledge on the role EPCs in four disorders with neurovascular involvement, which are Alzheimer’s disease, cerebral small vessel disease, ischemic stroke and migraine, with a particular focus on the potential practical use of these cells as a treatment remedy. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessReview

Coronary Microvascular Dysfunction in Diabetes Mellitus: Pathogenetic Mechanisms and Potential Therapeutic Options

and

Ferdinando Carlo Sasso

Biomedicines 2022, 10(9), 2274; https://doi.org/10.3390/biomedicines10092274 - 14 Sep 2022

Cited by 5 | Viewed by 1944

Abstract

Diabetic patients are frequently affected by coronary microvascular dysfunction (CMD), a condition consisting of a combination of altered vasomotion and long-term structural change to coronary arterioles leading to impaired regulation of blood flow in response to changing cardiomyocyte oxygen requirements. The pathogenesis of this microvascular complication is complex and not completely known, involving several alterations among which hyperglycemia and insulin resistance play particularly central roles leading to oxidative stress, inflammatory activation and altered barrier function of endothelium. CMD significantly contributes to cardiac events such as angina or infarction without obstructive coronary artery disease, as well as heart failure, especially the phenotype associated with preserved ejection fraction, which greatly impact cardiovascular (CV) prognosis. To date, no treatments specifically target this vascular damage, but recent experimental studies and some clinical investigations have produced data in favor of potential beneficial effects on coronary micro vessels caused by two classes of glucose-lowering drugs: glucagon-like peptide 1 (GLP-1)-based therapy and inhibitors of sodium-glucose cotransporter-2 (SGLT2). The purpose of this review is to describe pathophysiological mechanisms, clinical manifestations of CMD with particular reference to diabetes, and to summarize the protective effects of antidiabetic drugs on the myocardial microvascular compartment. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessReview

Endothelial Dysfunction, Erectile Deficit and Cardiovascular Disease: An Overview of the Pathogenetic Links

Federico De Leonardis

and

Anastasios D. Asimakopoulos

Biomedicines 2022, 10(8), 1848; https://doi.org/10.3390/biomedicines10081848 - 01 Aug 2022

Cited by 2 | Viewed by 1225

Abstract

Erectile dysfunction (ED) is a condition with multifactorial pathogenesis, quite common among men, especially those above 60 years old. A vascular etiology is the most common cause. The interaction between chronic inflammation, androgens, and cardiovascular risk factors determines macroscopically invisible alterations such as endothelial dysfunction and subsequent atherosclerosis and flow-limiting stenosis that affects both penile and coronary arteries. Thus, ED and cardiovascular disease (CVD) should be considered two different manifestations of the same systemic disorder, with a shared aetiological factor being endothelial dysfunction. Moreover, the penile arteries have a smaller size compared with coronary arteries; thus, for the same level of arteriopathy, a more significant blood flow reduction will occur in erectile tissue compared with coronary circulation. As a result, ED often precedes CVD by 2–5 years, and its diagnosis offers a time window for cardiovascular risk mitigation. Growing evidence suggests, in fact, that patients presenting with ED should be investigated for CVD even if they have no symptoms. Early detection could facilitate prompt intervention and a reduction in long-term complications. In this review, we provide an overview of the pathogenetic mechanisms behind arteriogenic ED and CVD, focusing on the role of endothelial dysfunction as the common denominator of the two disorders. Developed algorithms that may help identify those patients complaining of ED who should undergo detailed cardiologic assessment and receive intensive treatment for risk factors are also analyzed. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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Open AccessReview

The Role of KLF2 in the Regulation of Atherosclerosis Development and Potential Use of KLF2-Targeted Therapy

Siarhei A. Dabravolski

Vasily N. Sukhorukov

Vladislav A. Kalmykov

Andrey V. Grechko

Nikolay K. Shakhpazyan

and

Alexander N. Orekhov

Biomedicines 2022, 10(2), 254; https://doi.org/10.3390/biomedicines10020254 - 24 Jan 2022

Cited by 10 | Viewed by 3039

Abstract

Kruppel like factor 2 (KLF2) is a mechanosensitive transcription factor participating in the regulation of vascular endothelial cells metabolism. Activating KLF2 in endothelial cells induces eNOS (endothelial nitric oxide synthase) expression, subsequent NO (nitric oxide) release, and vasodilatory effect. In addition, many KLF2-regulated genes participate in the anti-thrombotic, antioxidant, and anti-inflammatory activities, thereby preventing atherosclerosis development and progression. In this review, we summarise recent evidence suggesting that KLF2 plays a major role in regulating atheroprotective effects in endothelial cells. We also discuss several recently identified repurposed drugs and natural plant-based bioactive compounds with KLF2-mediated atheroprotective activities. Herein, we present a comprehensive overview of the role of KLF2 in atherosclerosis and as a pharmacological target for different drugs and natural compounds and highlight the potential application of these phytochemicals for the treatment of atherosclerosis. Full article

(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Advances in Endothelial Dysfunction)

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