Anthracycline-Induced Cardiotoxicity: The Role of Endothelial Dysfunction

Cardiology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Elena V. Grakova ◽  
Sergey N. Shilov ◽  
Kristina V. Kopeva ◽  
Ekaterina N. Berezikova ◽  
Anna A. Popova ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Genetic Factors ◽  
Vascular Toxicity ◽  
Endothelin 1 ◽  
Endothelial Cell Death ◽  
Endothelial Nitric Oxide ◽  
Genetic Susceptibility Factor

Cardiovascular disease remains the leading cause of mortality accounting up to 40% of all deaths, but, currently, cancer is prominent cause of death globally. Anthracyclines are the cornerstone of chemotherapy in women with breast cancer. However, its clinical use is limited by their cardiotoxic effects that can trigger heart failure development. Vascular toxicity of chemotherapy may be linked with endothelial dysfunction because anthracycline damage of endothelial cells can lead to the development and progression of cardiomyopathy by decreasing the release and activity of endothelial factors and, ultimately, endothelial cell death. These processes suppress anti-inflammatory and vascular reparative functions and initiate the development of future cardiovascular events. Recent studies have shown that chemotherapy may induce toxicity in the vascular endothelium and is accompanied by systemic endothelial dysfunction in patients with diagnosed cardiovascular diseases. Because the initial endothelial cell insult is likely asymptomatic, there is often a long delay between the termination of doxorubicin therapy and the onset of vascular disorders. In this case, genetic susceptibility factor will help to identify susceptible patients in the future. The objectives of this study were to evaluate prognostic role of molecular (endothelin-1) and genetic factors (gene polymorphisms of endothelial nitric oxide (NO) synthase (NOS3, rs1799983), endothelin-1 receptor type A (EDNRA, C+70G, rs5335) and NADPH oxidase (C242T, rs4673) in development of endothelial dysfunction and anthracycline-induced cardiotoxicity in women without cardiovascular diseases.

scholarly journals Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 377
Author(s):  
Yunna Lee ◽  
Eunok Im
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Natural Antioxidants ◽  
Sirtuin 1 ◽  
Potential Benefits ◽  
New Perspective ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Cardiovascular diseases (CVDs) are the most common cause of morbidity and mortality worldwide. The potential benefits of natural antioxidants derived from supplemental nutrients against CVDs are well known. Remarkably, natural antioxidants exert cardioprotective effects by reducing oxidative stress, increasing vasodilation, and normalizing endothelial dysfunction. Recently, considerable evidence has highlighted an important role played by the synergistic interaction between endothelial nitric oxide synthase (eNOS) and sirtuin 1 (SIRT1) in the maintenance of endothelial function. To provide a new perspective on the role of natural antioxidants against CVDs, we focused on microRNAs (miRNAs), which are important posttranscriptional modulators in human diseases. Several miRNAs are regulated via the consumption of natural antioxidants and are related to the regulation of oxidative stress by targeting eNOS and/or SIRT1. In this review, we have discussed the specific molecular regulation of eNOS/SIRT1-related endothelial dysfunction and its contribution to CVD pathologies; furthermore, we selected nine different miRNAs that target the expression of eNOS and SIRT1 in CVDs. Additionally, we have summarized the alteration of miRNA expression and regulation of activities of miRNA through natural antioxidant consumption.

ENDOTHELIAL FUNCTION IN CHILDREN WITH PERIODONTITIS

2021 ◽  
pp. 154-161
Author(s):  
Agapitov L.I. ◽  
Cherepnina I.V.
Keyword(s):  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Chronic Periodontitis ◽  
Preventive Measures ◽  
Inverse Correlation ◽  
Healthy Children ◽  
Flow Mediated Dilatation ◽  
Vascular Dilatation ◽  
Oral Inflammation

The presence of oral inflammation has recently been linked with the pathogenesis of cardiovascular diseases. Endothelial dysfunction is considered one of the pathogenetic mechanisms of a whole range of cardiovascular diseases. In the study describes links between periodontitis and endothelial dysfunction. 32 patients (16 boys and 16 girls) with periodontitis and 60 healthy children were examined. Flow-mediated vascular dilatation data were measured in all patients. Flow-mediated dilatation was 9,78±3,16% in children with periodontitis, and 12,85±3,48% in healthy children (p<0,05). Area under the dilation curve was larger in healthy children, then in children with periodontitis, 710±121%·с in comparison with 519±175%·с (p<0,05). An inverse correlation was found between flow-mediated dilatation, area under the dilation curve and periodontitis duration (r = -0,71, -0,77). A negative correlation was found between flow-mediated dilatation, area under the dilation curve and worsening of periodontitis (r = -0,70, -0,71). This study did not demonstrate association between periodontal disease in children and arterial hypertension, coronary heart disease, heart failure. However, the identified endothelial dysfunction requires protective therapeutic and preventive measures. Given the insignificant symptoms of chronic periodontitis in the examined children, it is important to activate efforts aimed at early detection and treatment of this disease. Further research is needed to clarify the prognostic role of endothelial dysfunction in chronic periodontitis.

scholarly journals The Role of Uridine Adenosine Tetraphosphate in the Vascular System

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Takayuki Matsumoto ◽  
Rita C. Tostes ◽  
R. Clinton Webb
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Smooth Muscle Cells ◽  
Vascular Function ◽  
Purinergic Receptors ◽  
Potential Role ◽  
Vascular System

The endothelium plays a pivotal role in vascular homeostasis, and endothelial dysfunction is a major feature of cardiovascular diseases, such as arterial hypertension, atherosclerosis, and diabetes. Recently, uridine adenosine tetraphosphate (Up4A) has been identified as a novel and potent endothelium-derived contracting factor (EDCF). Up4A structurally contains both purine and pyrimidine moieties, which activate purinergic receptors. There is an accumulating body of evidence to show that Up4A modulates vascular function by actions on endothelial and smooth muscle cells. In this paper, we discuss the effects of Up4A on vascular function and a potential role for Up4A in cardiovascular diseases.

scholarly journals The Role of Endothelial Dysfunction in the Development of Cardiotoxic Action of Cytostatics in Patients with Lymphoproliferative Diseases

Kardiologiia ◽  
2019 ◽  
Vol 59 (4) ◽  
pp. 64-66 ◽  
Author(s):  
D. A. Budanova ◽  
Yu. N. Belenkov ◽  
I. Ya. Sokolova ◽  
O. N. Antyufeeva ◽  
V. I. Ershov ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Normal Values ◽  
Clear Understanding ◽  
Age Group ◽  
Lymphoproliferative Diseases ◽  
Endothelin 1 ◽  
Vasoconstrictor Effect ◽  
Before And After ◽  
Chemotherapy Cardiotoxicity

Understanding mechanisms of chemotherapy cardiotoxicity is an important problem due to the lack of clear understanding of its occurrence. Development of endothelial dysfunction is considered to be one of possible ways in implementation of these side effects. The analysis of endothelin-1 and e-selectin levels in 26  patients with lymphoproliferative diseases before and after the completion of the treatment program was been performed. The results of the study showed normal values of E-selectin level and increased level of endothelin-1 in the whole group of patients before treatment. After completion of chemotherapy program, in the whole group, there was a decrease of these two markers. However, values of level of endothelin-1 with vasoconstrictor effect remained high even after the end of therapy. It is imp ortant that at detailed analysis the dynamics of investigated markers in patients of older age group (median age 64 years) was associated with worsening of endothelial dysfunction.

scholarly journals Role of Endothelial Nitric Oxide Synthase in Endothelial Cell Migration

1999 ◽  
Vol 19 (5) ◽  
pp. 1156-1161 ◽  
Author(s):  
Toyoaki Murohara ◽  
Bernhard Witzenbichler ◽  
Ioakim Spyridopoulos ◽  
Takayuki Asahara ◽  
Bo Ding ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Endothelial Cell Migration ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Evolving Role of Microparticles in the Pathophysiology of Endothelial Dysfunction

2013 ◽  
Vol 59 (8) ◽  
pp. 1166-1174 ◽  
Author(s):  
Fina Lovren ◽  
Subodh Verma
Keyword(s):  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Vascular Endothelial Cells ◽  
Current Knowledge ◽  
Early Event ◽  
Prognostic Information ◽  
Vascular Events ◽  
Wide Range

BACKGROUND Endothelial dysfunction is an early event in the development and progression of a wide range of cardiovascular diseases. Various human studies have identified that measures of endothelial dysfunction may offer prognostic information with respect to vascular events. Microparticles (MPs) are a heterogeneous population of small membrane fragments shed from various cell types. The endothelium is one of the primary targets of circulating MPs, and MPs isolated from blood have been considered biomarkers of vascular injury and inflammation. CONTENT This review summarizes current knowledge of the potential functional role of circulating MPs in promoting endothelial dysfunction. Cells exposed to different stimuli such as shear stress, physiological agonists, proapoptotic stimulation, or damage release MPs, which contribute to endothelial dysfunction and the development of cardiovascular diseases. Numerous studies indicate that MPs may trigger endothelial dysfunction by disrupting production of nitric oxide release from vascular endothelial cells and subsequently modifying vascular tone. Circulating MPs affect both proinflammatory and proatherosclerotic processes in endothelial cells. In addition, MPs can promote coagulation and inflammation or alter angiogenesis and apoptosis in endothelial cells. SUMMARY MPs play an important role in promoting endothelial dysfunction and may prove to be true biomarkers of disease state and progression.

scholarly journals Concentrations of the Selected Biomarkers of Endothelial Dysfunction in Response to Antiepileptic Drugs: A Literature Review

2019 ◽  
Vol 25 ◽  
pp. 107602961985942 ◽  
Author(s):  
Beata Sarecka-Hujar ◽  
Izabela Szołtysek-Bołdys ◽  
Ilona Kopyta ◽  
Barbara Dolińska ◽  
Andrzej Sobczak
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Literature Review ◽  
Antiepileptic Drug ◽  
Asymmetric Dimethylarginine ◽  
The Body ◽  
Biochemical Processes ◽  
The Brain

Epilepsy is a disease arising from morphological and metabolic changes in the brain. Approximately 60% of patients with seizures can be controlled with 1 antiepileptic drug (AED), while in others, polytherapy is required. The AED treatment affects a number of biochemical processes in the body, including increasing the risk of cardiovascular diseases (CVDs). It is indicated that the duration of AED therapy with some AEDs significantly accelerates the process of atherosclerosis. Most of AEDs increase levels of homocysteine (HCys) as well as may affect concentrations of new, nonclassical risk factors for atherosclerosis, that is, asymmetric dimethylarginine (ADMA) and homoarginine (hArg). Because of the role of these parameters in the pathogenesis of CVD, knowledge of HCys, ADMA, and hArg concentrations in patients with epilepsia treated with AED, both pediatric and adult, appears to be of significant importance.

Role of Endothelin-1 and Endothelial Dysfunction in Prehypertension

2012 ◽  
Vol 28 (3) ◽  
pp. 251-253 ◽  
Author(s):  
Christine K. Kissel ◽  
Todd J. Anderson
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelin 1

scholarly journals Expression of Endothelial Nitric Oxide Synthase and Endothelin-1 in Skin Tissue from Amputated Limbs of Patients with Complex Regional Pain Syndrome

2008 ◽  
Vol 2008 ◽  
pp. 1-5 ◽  
Author(s):  
J. George Groeneweg ◽  
Claudia Heijmans Antonissen ◽  
Frank J. P. M. Huygen ◽  
Freek J. Zijlstra
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Complex Regional Pain Syndrome ◽  
Endothelial Nitric Oxide Synthase ◽  
Pain Syndrome ◽  
Skin Tissue ◽  
Endothelin 1 ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background and Objectives. Impaired microcirculation during the chronic stage of complex regional pain syndrome (CRPS) is related to increased vasoconstriction, tissue hypoxia, and metabolic tissue acidosis in the affected limb. Endothelial dysfunction is suggested to be the main cause of diminished blood flow. The aim of this study was to examine the distribution of endothelial nitric oxide synthase (eNOS) and endothelin-1(ET-1) relative to vascular density represented by the endothelial marker CD31-immunoreactivity in the skin tissue of patients with chronic CRPS.Methods. We performed immunohistochemical staining on sections of skin specimens obtained from the amputated limbs (one arm and one leg) of two patients with CRPS.Results. In comparison to proximal specimens we found an increased number of migrated endothelial cells as well as an increase of eNOS activity in distal dermis specimens.Conclusions. We found indications that endothelial dysfunction plays a role in chronic CRPS.

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