Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
4.7
Journals
Biomedicines
Special Issues
Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic...
share announcement

Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II)

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 March 2023) | Viewed by 19822

Special Issue Editors

Prof. Dr. Guido Grassi

E-Mail Website
Guest Editor
Department of Clinical Medicine, Prevention and Health Biotechnology, San Gerardo Hospital, University of Milan-Bicocca, Via G. B. Pergolesi, 33, 20900 Monza, MB, Italy
Interests: cardiovascular disease; metabolic syndrome; diabetes
Special Issues, Collections and Topics in MDPI journals
Dr. Pasquale Ambrosino

E-Mail Website
Guest Editor
Istituti Clinici Scientifici Maugeri IRCCS, Pavia, Italy
Interests: cardiovascular risk; endothelial function; arterial stiffness; atherosclerosis; COVID-19; chronic obstructive pulmonary disease; asthma; biomarkers; rehabilitation; chronic disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is the second volume of the Special Issue "Endothelial dysfunction: from a pathophysiological mechanism to a potential therapeutic target".

Endothelial cells are able to respond to a number of chemical signals by producing a wide range of mediators regulating vascular tone, cellular adhesion, coagulation, smooth muscle cell proliferation, and vessel wall inflammation.

Under normal conditions, endothelium-derived nitric oxide (NO) plays a key role in vascular and airway homeostasis by inhibiting inflammation and oxidative stress. However, a number of both NO-dependent and NO-independent pathways have been called into question to explain the regulatory role of the endothelium.

Endothelial dysfunction is the earliest stage of the atherosclerotic process and even a trigger of cardiovascular (CV) events. Moreover, the presence of a dysfunctional endothelium has been proposed as a key and early pathogenic mechanism in many acute and chronic diseases, including the novel Coronavirus Disease 2019 (COVID-19).

The leading role of endothelial function in vascular and organ homeostasis led to the development of many clinical and laboratory tests for its assessment (e.g., flow-mediated dilation). Similarly, different techniques have been tested to measure NO in biological samples. Moreover, due to its systemic nature and reversibility in early stages, endothelial dysfunction has been proposed as an attractive therapeutic target in many clinical conditions, with a potential emerging role for specific pharmacological interventions and tailored exercise-based rehabilitation strategies.

This Special Issue will focus on the mechanisms and diagnosis, as well as the prognostic and therapeutic implications of endothelial dysfunction as a biomarker of inflammation, oxidative stress, and vascular disease. The Special Issue is open for both basic and clinical research or for omics-based and translational approaches and will cover original articles as well as reviews and a limited number of pertinent meta-analyses.

Prof. Dr. Guido Grassi
Dr. Pasquale Ambrosino
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 2600 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 function
  • nitric oxide
  • reactive oxygen species
  • flow-mediated dilation
  • cardiovascular risk
  • vascular medicine
  • inflammation
  • biomarkers

Published Papers (10 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

5 pages, 220 KiB  
Editorial
Is It All about Endothelial Dysfunction? Focusing on the Alteration in Endothelial Integrity as a Key Determinant of Different Pathological Mechanisms
by Pasquale Ambrosino, Silvestro Ennio D’Anna, Guido Grassi and Mauro Maniscalco
Biomedicines 2022, 10(11), 2757; https://doi.org/10.3390/biomedicines10112757 - 31 Oct 2022
Cited by 1 | Viewed by 989
Abstract
The endothelium is composed of a monolayer of endothelial cells (ECs) covering the inner side of arterial, venous and lymphatic vessels [...] Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))

Research

Jump to: Editorial, Review

18 pages, 13299 KiB  
Article
Dimethyloxalylglycine Attenuates Steroid-Associated Endothelial Progenitor Cell Impairment and Osteonecrosis of the Femoral Head by Regulating the HIF-1α Signaling Pathway
by Wenkai Shao, Zilin Li, Bo Wang, Song Gong, Ping Wang, Beite Song, Zhixiang Chen and Yong Feng
Biomedicines 2023, 11(4), 992; https://doi.org/10.3390/biomedicines11040992 - 23 Mar 2023
Cited by 3 | Viewed by 1480
Abstract
Endothelial impairment and dysfunction are closely related to the pathogenesis of steroid-associated osteonecrosis of the femoral head (SONFH). Recent studies have showed that hypoxia inducible factor-1α (HIF-1α) plays a crucial role in endothelial homeostasis maintenance. Dimethyloxalylglycine (DMOG) could suppress HIF-1 degradation and result [...] Read more.
Endothelial impairment and dysfunction are closely related to the pathogenesis of steroid-associated osteonecrosis of the femoral head (SONFH). Recent studies have showed that hypoxia inducible factor-1α (HIF-1α) plays a crucial role in endothelial homeostasis maintenance. Dimethyloxalylglycine (DMOG) could suppress HIF-1 degradation and result in nucleus stabilization by repressing prolyl hydroxylase domain (PHD) enzymatic activity. Our results showed that methylprednisolone (MPS) remarkably undermined biological function of endothelial progenitor cells (EPC) by inhibiting colony formation, migration, angiogenesis, and stimulating senescence of EPCs, while DMOG treatment alleviated these effects by promoting HIF-1α signaling pathway, as evidenced by senescence-associated β-galactosidase (SA-β-Gal) staining, colony-forming unit, matrigel tube formation, and transwell assays. The levels of proteins related to angiogenesis were determined by ELISA and Western blotting. In addition, active HIF-1α bolstered the targeting and homing of endogenous EPCs to the injured endothelium in the femoral head. Histopathologically, our in vivo study showed that DMOG not only alleviated glucocorticoid-induced osteonecrosis but also promoted angiogenesis and osteogenesis in the femoral head as detected by microcomputed tomography (Micro-CT) analysis and histological staining of OCN, TRAP, and Factor Ⅷ. However, all of these effects were impaired by an HIF-1α inhibitor. These findings demonstrate that targeting HIF-1α in EPCs may constitute a novel therapeutic approach for the treatment of SONFH. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

16 pages, 23428 KiB  
Article
Sesamin Attenuates VEGFA-Induced Angiogenesis via Inhibition of Src and FAK Signaling in Chick Chorioallantoic Membrane Model and Human Endothelial EA.hy926 Cells
by Tanyaporn Keratibumrungpong, Warunee Srisuthtayanont, Orawan Wanachewin, Jeerawan Klangjorhor, Thanyaluck Phitak, Peraphan Pothacharoen, Thuzar Hla Shwe and Prachya Kongtawelert
Biomedicines 2023, 11(1), 188; https://doi.org/10.3390/biomedicines11010188 - 11 Jan 2023
Cited by 1 | Viewed by 1544
Abstract
Sesamin, a major phytochemical in sesame seeds and oil, has been reported to have effects on physiological and pathological angiogenesis in several studies. Nevertheless, the underlying mechanisms of sesamin’s effect on angiogenesis are not understood well enough. This study aimed to investigate its [...] Read more.
Sesamin, a major phytochemical in sesame seeds and oil, has been reported to have effects on physiological and pathological angiogenesis in several studies. Nevertheless, the underlying mechanisms of sesamin’s effect on angiogenesis are not understood well enough. This study aimed to investigate its effect on both physiological and pathological angiogenesis using the in vivo chick chorioallantoic membrane (CAM) model and the in vitro human endothelial cell line, EA.hy926, model. Sesamin inhibited the VEGFA-induced pathological angiogenesis significantly, although no effect was seen on angiogenesis without induction. It reduced the formation of vascular branches in the VEGFA-treated CAMs and also the proliferation and migration of EA.hy926 endothelial cells induced by VEGFA. Sesamin impeded the VEGF-mediated activation of Src and FAK signaling proteins, which may be responsible for sesamin-mediated reduction of pathological angiogenesis. Moreover, the effect of sesamin on the expressions of angiogenesis-related genes was then investigated and it was found that both mRNA and protein expressions of Notch1, the key pathway in vascular development, induced by VEGFA, were significantly reduced by sesamin. Our results altogether suggested that sesamin, by inhibiting pathological angiogenesis, has the potential to be employed in the prevention or treatment of diseases with over-angiogenesis, such as cancers. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

18 pages, 2834 KiB  
Article
Brain Protective Effect of Resveratrol via Ameliorating Interleukin-1β-Induced MMP-9-Mediated Disruption of ZO-1 Arranged Integrity
by Ming-Ming Tsai, Jiun-Liang Chen, Tsong-Hai Lee, Hsiuming Liu, Velayuthaprabhu Shanmugam and Hsi-Lung Hsieh
Biomedicines 2022, 10(6), 1270; https://doi.org/10.3390/biomedicines10061270 - 29 May 2022
Cited by 5 | Viewed by 2269
Abstract
In the central nervous system (CNS), the matrix metalloproteinase-9 (MMP-9) is induced by several factors and contributes to CNS disorders, including inflammation and neurodegeneration. Thus, the upregulation of MMP-9 has been considered to be an indicator of inflammation. Interleukin-1β (IL-1β) is an important [...] Read more.
In the central nervous system (CNS), the matrix metalloproteinase-9 (MMP-9) is induced by several factors and contributes to CNS disorders, including inflammation and neurodegeneration. Thus, the upregulation of MMP-9 has been considered to be an indicator of inflammation. Interleukin-1β (IL-1β) is an important proinflammatory cytokine which can induce various inflammatory factors, such as MMP-9, in many inflammatory disorders. Several phytochemicals are believed to reduce the risk of several inflammatory disorders, including the CNS diseases. Among them, the resveratrol, a principal phenolic compound of the grape, blueberry, and mulberry peels and Cassia plants, has been shown to possess several medicinal properties, including antioxidative, anti-inflammatory, and antitumor function. Herein, we used mouse-brain microvascular endothelial cells (bMECs) to demonstrate the signaling mechanisms of IL-1β-induced MMP-9 expression via zymographic, RT-PCR, Western blot, reactive oxygen species (ROS) detection, immunofluorescence stain, and promoter reporter analyses. Then we evaluated the effects of resveratrol on IL-1β-induced MMP-9 expression in bMECs and its mechanism of action. We first demonstrated that IL-1β induced MMP-9 expression in bMECs. Subsequently, IL-1β induced MMP-9 expression via ROS-mediated c-Src-dependent transactivation of EGFR, and then activation of the ERK1/2, p38 MAPK, JNK1/2, and NF-κB signaling pathway. Finally, we determined that IL-1β-induced upregulation of MMP-9 may cause the disruption of the arranged integrity of zonula occludens-1 (ZO-1), but this could be inhibited by resveratrol. These data indicated that resveratrol may have antioxidative and brain-protective activities by reducing these related pathways of ROS-mediated MMP-9 expression and tight junction disruption in brain microvascular endothelial cells. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

11 pages, 269 KiB  
Article
Blood M2-like Monocyte Polarization Is Associated with Calcific Plaque Phenotype in Stable Coronary Artery Disease: A Sub-Study of SMARTool Clinical Trial
by Silverio Sbrana, Antonella Cecchettini, Luca Bastiani, Nicoletta Di Giorgi, Annamaria Mazzone, Elisa Ceccherini, Federico Vozzi, Chiara Caselli, Danilo Neglia, Alberto Clemente, Arthur J. H. A. Scholte, Oberdan Parodi, Gualtiero Pelosi and Silvia Rocchiccioli
Biomedicines 2022, 10(3), 565; https://doi.org/10.3390/biomedicines10030565 - 28 Feb 2022
Cited by 3 | Viewed by 1949
Abstract
Background: Atherosclerosis is a chronic inflammatory disease. The balance between pro- and anti-inflammatory factors, acting on the arterial wall, promotes less or more coronary plaque macro-calcification, respectively. We investigated the association between monocyte phenotypic polarization and CTCA-assessed plaque dense-calcium volume (DCV) in patients [...] Read more.
Background: Atherosclerosis is a chronic inflammatory disease. The balance between pro- and anti-inflammatory factors, acting on the arterial wall, promotes less or more coronary plaque macro-calcification, respectively. We investigated the association between monocyte phenotypic polarization and CTCA-assessed plaque dense-calcium volume (DCV) in patients with stable coronary artery disease (CAD). Methods: In 55 patients, individual DCV component was assessed by quantitative CTCA and normalized to total plaque volume. Flow cytometry expression of CD14, CD16, CD18, CD11b, HLA-DR, CD163, CCR2, CCR5, CX3CR1 and CXCR4 was quantified. Adhesion molecules and cytokines were measured by ELISA. Results: DCV values were significantly associated, by multiple regression analysis, with the expression (RFI) of CCR5 (p = 0.04), CX3CR1 (p = 0.03), CCR2 (p = 0.02), CD163 (p = 0.005) on all monocytes, and with the phenotypic M2-like polarization ratio, RFI CCR5/CD11b (p = 0.01). A positive correlation with the increased expression of chemokines receptors CCR2, CCR5 and CX3CR1 on subsets Mon1 was also present. Among cytokines, the ratio between IL-10 and IL-6 was found to be strongly associated with DCV (p = 0.009). Conclusions: The association between DCV and M2-like phenotypic polarization of circulating monocytes indicates that plaque macro-calcification in stable CAD may be partly modulated by an anti-inflammatory monocyte functional state, as evidenced by cell membrane receptor patterns. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
10 pages, 1386 KiB  
Communication
Effect of Revascularization on Intramuscular Vascular Endothelial Growth Factor Levels in Peripheral Arterial Disease
by Larissa Schawe, Ben Raude, Jan Christoph Carstens, Irene Hinterseher, Raphael Donatus Hein, Safwan Omran, Gilles Berger, Nina A. Hering, Matthias Buerger, Andreas Greiner and Jan Paul Frese
Biomedicines 2022, 10(2), 471; https://doi.org/10.3390/biomedicines10020471 - 17 Feb 2022
Cited by 1 | Viewed by 1472
Abstract
Vascular endothelial growth factor (VEGF) is a potent driver of angiogenesis, which may help to relieve ischemia in peripheral arterial disease (PAD). We aimed to investigate the role of intramuscular VEGF in ischemic and non-ischemic skeletal muscle in PAD patients before and after [...] Read more.
Vascular endothelial growth factor (VEGF) is a potent driver of angiogenesis, which may help to relieve ischemia in peripheral arterial disease (PAD). We aimed to investigate the role of intramuscular VEGF in ischemic and non-ischemic skeletal muscle in PAD patients before and after surgical or endovascular revascularization and different stages of PAD. Biopsies of the gastrocnemius and vastus muscles from twenty PAD patients with stenosis or occlusion of the superficial femoral artery were obtained both during revascularization and 8 weeks postoperatively. The gastrocnemius muscle was considered ischemic, while vastus muscle biopsies served as intraindividual controls. The levels of vascular endothelial growth factor in muscle lysates were then determined by ELISA. Preoperative VEGF levels were significantly higher in ischemic muscles compared to the controls (98.07 ± 61.96 pg/mL vs. 55.50 ± 27.33 pg/mL, p = 0.004). Postoperative values decreased significantly (p = 0.010) to 54.83 ± 49.60 pg/mL in gastrocnemius biopsies. No significant change was observed in vastus muscle biopsies, with mean postoperative VEGF values found at 54.16 ± 40.66 pg/mL. Since all patients still had indications for revascularization, impairment of angiogenesis mechanisms can be assumed. More research about angiogenesis in PAD is needed with the ultimate goal to improve conservative treatment. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

19 pages, 3083 KiB  
Article
Uremic Toxin Lanthionine Induces Endothelial Cell Mineralization In Vitro
by Annapaola Coppola, Carmela Vigorito, Patrizia Lombari, Yuselys García Martínez, Margherita Borriello, Francesco Trepiccione, Diego Ingrosso and Alessandra F. Perna
Biomedicines 2022, 10(2), 444; https://doi.org/10.3390/biomedicines10020444 - 14 Feb 2022
Cited by 3 | Viewed by 2163
Abstract
Vascular calcification (VC) is a pathological event caused by the unusual deposition of minerals in the vascular system, representing the leading cause of cardiovascular mortality in chronic kidney disease (CKD). In CKD, the deregulation of calcium and phosphate metabolism, along with the effect [...] Read more.
Vascular calcification (VC) is a pathological event caused by the unusual deposition of minerals in the vascular system, representing the leading cause of cardiovascular mortality in chronic kidney disease (CKD). In CKD, the deregulation of calcium and phosphate metabolism, along with the effect of several uremic toxins, act as key processes conveying altered mineralization. In this work, we tested the ability of lanthionine, a novel uremic toxin, to promote calcification in human endothelial cell cultures (Ea.hy926). We evaluated the effects of lanthionine, at a concentration similar to that actually detected in CKD patients, alone and under pro-calcifying culture conditions using calcium and phosphate. In pro-calcific culture conditions, lanthionine increased both the intracellular and extracellular calcium content and induced the expression of Bone Morphogenetic Protein 2 (BMP2) and RUNX Family Transcription Factor 2 (RUNX2). Lanthionine treatment, in pro-calcifying conditions, raised levels of tissue-nonspecific alkaline phosphatase (ALPL), whose expression also overlapped with Dickkopf WNT Signaling Pathway Inhibitor 1 (DKK1) gene expression, suggesting a possible role of the latter gene in the activation of ALPL. In addition, treatment with lanthionine alone or in combination with calcium and phosphate reduced Inorganic Pyrophosphate Transport Regulator (ANKH) gene expression, a protective factor toward the mineralizing process. Moreover, lanthionine in a pro-calcifying condition induced the activation of ERK1/2, which is not associated with an increase in DKK1 protein levels. Our data underscored a link between mineral disease and the alterations of sulfur amino acid metabolisms at a cell and molecular level. These results set the basis for the understanding of the link between uremic toxins and mineral-bone disorder during CKD progression. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

16 pages, 2676 KiB  
Article
Sodium Accumulation and Blood Capillary Rarefaction in the Skin Predispose Spontaneously Hypertensive Rats to Salt Sensitive Hypertension
by Jan Šilhavý, Petr Mlejnek, Miroslava Šimáková, František Liška, Jan Kubovčiak, Eva Sticová and Michal Pravenec
Biomedicines 2022, 10(2), 376; https://doi.org/10.3390/biomedicines10020376 - 04 Feb 2022
Cited by 4 | Viewed by 1805
Abstract
Recent studies in humans and rats suggested that increased Na+ storage in the skin without parallel water retention may predispose to salt-sensitive hypertension. In the current studies, we compared tissue Na+ storage in salt sensitive spontaneously hypertensive rats (SHR) versus salt [...] Read more.
Recent studies in humans and rats suggested that increased Na+ storage in the skin without parallel water retention may predispose to salt-sensitive hypertension. In the current studies, we compared tissue Na+ storage in salt sensitive spontaneously hypertensive rats (SHR) versus salt resistant normotensive Brown Norway (BN-Lx) rats. After salt loading (10 days drinking 1% NaCl solution), the SHR showed significant parallel increase in Na+-to-water as well as (Na++K+)-to-water ratios suggesting increased storage of osmotically inactive Na+ in the skin while no significant changes in skin electrolyte concentrations were observed in BN-Lx rats. SHR rats after salt treatment exhibited a nonsignificant decrease in skin blood capillary number (rarefaction) while BN-Lx rats showed significantly increased skin blood capillary density. Analysis of dermal gene expression profiles in BN-Lx rats after salt treatment showed significant up-regulation of genes involved in angiogenesis and proliferation of endothelial cells contrary to the SHR. Since the skin harbors most of the body’s resistance vessels it is possible that blood capillary rarefaction may lead to increased peripheral resistance and salt sensitivity in the SHR. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

10 pages, 886 KiB  
Review
Endothelial, Vascular and Sympathetic Alterations as Therapeutic Targets in Chronic Heart Failure
by Fosca Quarti-Trevano, Raffaella Dell’Oro, Cesare Cuspidi, Pasquale Ambrosino and Guido Grassi
Biomedicines 2023, 11(3), 803; https://doi.org/10.3390/biomedicines11030803 - 06 Mar 2023
Cited by 2 | Viewed by 1474
Abstract
Vascular and sympathetic abnormalities characterize chronic heart failure (CHF). Alterations include (1) a reduction in arterial distensibility, (2) endothelial dysfunction, (3) a decrease in arterial compliance and a parallel increase in arterial stiffness, and (4) sympathetic cardiovascular activation. Altogether, these alterations represent important [...] Read more.
Vascular and sympathetic abnormalities characterize chronic heart failure (CHF). Alterations include (1) a reduction in arterial distensibility, (2) endothelial dysfunction, (3) a decrease in arterial compliance and a parallel increase in arterial stiffness, and (4) sympathetic cardiovascular activation. Altogether, these alterations represent important targets in therapeutic interventions, because they display an independent negative impact on the disease prognosis, favouring disease progression and the development of cardiovascular complications with direct and indirect mechanisms. The present review will examine the effects of the different therapeutic interventions targeting the vascular/sympathetic alterations detected in CHF. Non-pharmacological, pharmacological and device-based treatments will be discussed in detail, highlighting the possible mechanisms responsible for the vascular/sympathetic effects of each intervention. Finally, the unmet goals in treatment in relation to endothelial and adrenergic targets will be also discussed. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

19 pages, 1888 KiB  
Review
Obesity and Endothelial Function
by Masato Kajikawa and Yukihito Higashi
Biomedicines 2022, 10(7), 1745; https://doi.org/10.3390/biomedicines10071745 - 19 Jul 2022
Cited by 18 | Viewed by 3647
Abstract
Obesity is a major public health problem and is related to increasing rates of cardiovascular morbidity and mortality. Over 1.9 billion adults are overweight or obese worldwide and the prevalence of obesity is increasing. Obesity influences endothelial function through obesity-related complications such as [...] Read more.
Obesity is a major public health problem and is related to increasing rates of cardiovascular morbidity and mortality. Over 1.9 billion adults are overweight or obese worldwide and the prevalence of obesity is increasing. Obesity influences endothelial function through obesity-related complications such as hypertension, dyslipidemia, diabetes, metabolic syndrome, and obstructive sleep apnea syndrome. The excess fat accumulation in obesity causes adipocyte dysfunction and induces oxidative stress, insulin resistance, and inflammation leading to endothelial dysfunction. Several anthropometric indices and imaging modalities that are used to evaluate obesity have demonstrated an association between obesity and endothelial function. In the past few decades, there has been great focus on the mechanisms underlying endothelial dysfunction caused by obesity for the prevention and treatment of cardiovascular events. This review focuses on pathophysiological mechanisms of obesity-induced endothelial dysfunction and therapeutic targets of obesity. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: From a Pathophysiological Mechanism to a Potential Therapeutic Target (Volume II))
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-10
Back to TopTop