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Role of insulin, adenosine, and adipokine receptors in the foetoplacental vascular dysfunction in gestational diabetes mellitus.
Subiabre, M, Villalobos-Labra, R, Silva, L, Fuentes, G, Toledo, F, Sobrevia, L
Biochimica et biophysica acta. Molecular basis of disease. 2020;(2):165370
Abstract
Gestational diabetes mellitus (GDM) is a disease of pregnancy associated with maternal and foetal hyperglycaemia and altered foetoplacental vascular function. Human foetoplacental microvascular and macrovascular endothelium from GDM pregnancy show increased maximal l-arginine transport capacity via the human cationic amino acid transporter 1 (hCAT-1) isoform and nitric oxide (NO) synthesis by the endothelial NO synthase (eNOS). These alterations are paralleled by lower maximal transport activity of the endogenous nucleoside adenosine via the human equilibrative nucleoside transporter 1 (hENT1) and activation of adenosine receptors. A causal relationship has been described for adenosine-activation of A2A adenosine receptors, hCAT-1, and eNOS activity (i.e. the Adenosine/l-Arginine/Nitric Oxide, ALANO, signalling pathway). Insulin restores these alterations in GDM via activation of insulin receptor A (IR-A) form in the macrovascular but IR-A and IR-B forms in the microcirculation of the human placenta. Adipokines are secreted from adipocytes influencing the foetoplacental metabolic and vascular function. Various adipokines are dysregulated in GDM, with adiponectin and leptin playing major roles. Abnormal plasma concentration of these adipokines and the activation or their receptors are involved in the pathophysiology of GDM. However, involvement of adipokines, adenosine, and insulin receptors and membrane transporters in the aetiology of this disease of pregnancy is unknown. This review focuses on the pathophysiology of insulin and adenosine receptors and l-arginine and adenosine membranes transporters giving an overview of the key adipokines leptin and adiponectin in the foetoplacental vasculature in GDM. This article is part of a Special Issue entitled: Membrane Transporters and Receptors in Pregnancy Metabolic Complications edited by Luis Sobrevia.
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2.
Vitamin D deficiency in association with endothelial dysfunction: Implications for patients with COVID-19.
Zhang, J, McCullough, PA, Tecson, KM
Reviews in cardiovascular medicine. 2020;(3):339-344
Abstract
There is emerging evidence to suggest that vitamin D deficiency is associated with adverse outcomes in COVID-19 patients. Conversely, vitamin D supplementation protects against an initial alveolar diffuse damage of COVID-19 becoming progressively worse. The mechanisms by which vitamin D deficiency exacerbates COVID-19 pneumonia remain poorly understood. In this review we describe the rationale of the putative role of endothelial dysfunction in this event. Herein, we will briefly review (1) anti-inflammatory and anti-thrombotic effects of vitamin D, (2) vitamin D receptor and vitamin D receptor ligand, (3) protective role of vitamin D against endothelial dysfunction, (4) risk of vitamin D deficiency, (5) vitamin D deficiency in association with endothelial dysfunction, (6) the characteristics of vitamin D relevant to COVID-19, (7) the role of vitamin D on innate and adaptive response, (8) biomarkers of endothelial cell activation contributing to cytokine storm, and (9) the bidirectional relationship between inflammation and homeostasis. Finally, we hypothesize that endothelial dysfunction relevant to vitamin D deficiency results from decreased binding of the vitamin D receptor with its ligand on the vascular endothelium and that it may be immune-mediated via increased interferon 1 α. A possible sequence of events may be described as (1) angiotensin II converting enzyme-related initial endothelial injury followed by vitamin D receptor-related endothelial dysfunction, (2) endothelial lesions deteriorating to endothelialitis, coagulopathy and thrombosis, and (3) vascular damage exacerbating pulmonary pathology and making patients with vitamin D deficiency vulnerable to death.
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3.
Mediterranean Diet and Endothelial Function: A Review of its Effects at Different Vascular Bed Levels.
Torres-Peña, JD, Rangel-Zuñiga, OA, Alcala-Diaz, JF, Lopez-Miranda, J, Delgado-Lista, J
Nutrients. 2020;(8)
Abstract
The Mediterranean diet has recently been the focus of considerable attention as a palatable model of a healthy diet. Its influence on many cardiovascular risk factors, combined with its proven effect in reducing the risk of cardiovascular events in primary prevention, has boosted scientific interest in this age-old nutritional model. Many of the underlying mechanisms behind its health-giving effects have been revealed, from the modulation of the microbiota to the function of high-density lipoproteins (HDL), and it seems to deliver its health benefits mainly by regulating several key mechanisms of atherosclerosis. In this review, we will review the evidence for its regulation of endothelial function, a key element in the early and late stages of atherosclerosis. In addition, we will assess studies which evaluate its effects on the functioning of different arterial territory vessels (mainly the microvascular, peripheral and central vascular beds), focusing mainly on the capillary, brachial and carotid arteries. Finally, we will evaluate the molecular mechanisms which may be involved.
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Coffee and Endothelial Function: A Coffee Paradox?
Higashi, Y
Nutrients. 2019;(9)
Abstract
Coffee is a popular beverage throughout the world. Coffee contains various chemical compounds (e.g., caffeine, chlorogenic acids, hydroxyhydroquinone, kahweol, cafestol, and complex chemical mixtures). Caffeine is also the most widely consumed pharmacological substance in the world and is included in various beverages (e.g., coffee, tea, soft drinks, and energy drinks), products containing chocolate, and drugs. The effects of coffee and caffeine on cardiovascular diseases remain controversial. It is well known that there are J-curve-type or U-curve-type associations of coffee consumption with cardiovascular events including myocardial infarction and stroke. However, there is little information on the direct and indirect effects of coffee consumption on endothelial function in humans. It is likely that the coffee paradox or caffeine paradox exists the association of coffee intake with cardiovascular diseases, cardiovascular outcomes, and endothelial function. This review focusses on the effects of coffee and caffeine on endothelial function from molecular mechanisms to clinical perspectives.
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Polyphenols Regulate Endothelial Functions and Reduce the Risk of Cardiovascular Disease.
Yamagata, K
Current pharmaceutical design. 2019;(22):2443-2458
Abstract
BACKGROUND Previous studies have shown that intake of polyphenols through the consumption of vegetables and fruits reduces the risk of Cardiovascular Disease (CVD) by potentially influencing endothelial cell function. OBJECTIVE In this review, the effects and molecular mechanisms of plant polyphenols, particularly resveratrol, epigallocatechin gallate (EGCG), and quercetin, on endothelial functions, and their putative protective effects against CVD are described. METHODS Epidemiologic studies examined the effect of the CVD risk of vegetables and the fruit. Furthermore, studies within vitro models investigated the underlying molecular mechanisms of the action of the flavonoid class of polyphenols. These findings help elucidate the effect of polyphenols on endothelial function and CVD risk reduction. RESULTS Epidemiologic and in vitro studies have demonstrated that the consumption of vegetables and fruits decreases the incidence of CVDs. Furthermore, it has also been indicated that dietary polyphenols are inversely related to the risk of CVD. Resveratrol, EGCG, and quercetin prevent oxidative stress by regulating the expression of oxidase and the antioxidant enzyme genes, contributing to the prevention of stroke, hypertension, heart failure, and ischemic heart disease. CONCLUSION High intake of dietary polyphenols may help prevent CVD. Polyphenols inhibit endothelial dysfunction and induce vascular endothelium-dependent vascular relaxation viz. redox regulation and nitric oxide production. The polyphenol-induced healthy endothelial cell function may be related to CVD prevention.
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Is Heart Failure with Preserved Ejection Fraction a Kidney Disorder?
Shah, KS, Fang, JC
Current hypertension reports. 2019;(11):86
Abstract
PURPOSE OF REVIEW Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome of exertional intolerance, cardiac dysfunction, and fluid overload and is associated with significant morbidity and mortality. RECENT FINDINGS As our understanding of this syndrome has evolved, we are beginning to recognize the similarities and associations with chronic kidney disease (CKD). Salt and fluid retention are common in CKD and may be the sentinel event leading ultimately to the syndrome of HFpEF. Mechanisms linking both disease states include hypervolemia, inflammation, and endothelial dysfunction, which are also common to comorbidities that drive both HFpEF and CKD. In this review, we will discuss recent clinical research focusing on HFpEF, CKD, and comorbidities including hypertension and diabetes mellitus. We will review strategies for volume management and novel therapeutic approaches with new classes of drugs, including sodium-glucose cotransporters and angiotensin receptor/neprilysin inhibitors, which may work through targeting of both the heart and the kidney. Lastly, we emphasize why focusing on the alleviation of factors provoking renal injury and slowing the progression of renal dysfunction may provide the most therapeutic benefit in patients who have been diagnosed with HFpEF.
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Microvascular Vasodilator Plasticity After Acute Exercise.
Robinson, AT, Fancher, IS, Mahmoud, AM, Phillips, SA
Exercise and sport sciences reviews. 2018;(1):48-55
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Abstract
Endothelium-dependent vasodilation is reduced after acute exercise or after high intraluminal pressure in isolated arterioles from sedentary adults but not in arterioles from regular exercisers. The preserved vasodilation in arterioles from exercisers is hydrogen peroxide (H2O2) dependent, whereas resting dilation is nitric oxide (NO) dependent. We hypothesize chronic exercise elicits adaptations allowing for maintained vasodilation when NO bioavailability is reduced.
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The Effects of Flavonoids on Cardiovascular Health: A Review of Human Intervention Trials and Implications for Cerebrovascular Function.
Rees, A, Dodd, GF, Spencer, JPE
Nutrients. 2018;(12)
Abstract
Research has suggested a number of beneficial effects arising from the consumption of dietary flavonoids, found in foods such as cocoa, apples, tea, citrus fruits and berries on cardiovascular risk factors such as high blood pressure and endothelial dysfunction. These effects are thought to have a significant impact upon both vascular and cerebrovascular health, ultimately with the potential to prevent cardiovascular and potentially neurodegenerative disease with a vascular component, for example vascular dementia. This review explores the current evidence for the effects of flavonoid supplementation on human endothelial function and both peripheral and cerebral blood flow (CBF). Evidence presented includes their potential to reduce blood pressure in hypertensive individuals, as well as increasing peripheral blood perfusion and promoting CBF in both healthy and at-risk populations. However, there is great variation in the literature due to the heterogeneous nature of the randomised controlled trials conducted. As such, there is a clear need for further research and understanding within this area in order to maximise potential health benefits.
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[Significance of Homocysteine in Glaucoma].
Jünemann, A, Rejdak, R, Hohberger, B
Klinische Monatsblatter fur Augenheilkunde. 2018;(2):163-174
Abstract
Endothelial dysfunction and vascular dysregulation play a role in the multifactorial pathogenesis of glaucomatous optic nerve atrophy. Hyperhomocysteinemia is a risk factor for endothelial dysfunction and is associated with primary open-angle glaucoma as well as secondary open-angle glaucoma in the pseudoexfoliation syndrome. This paper reviews the literature on the association between homocysteine metabolism and glaucomatous disease and explains the possible role of hyperhomocysteinemia in the pathogenesis and progression of glaucoma. We discuss the role of exogenous modifiable risk factors for the prevention and therapy of glaucoma, as well as modification of these factors by changes in life style, such as weight reduction, changes in nutrition and physical activity. The roles of homocysteine in regulating the extracellular matrix, vasotoxicity, neurodegeneration, and epigenetics are explained. Prevention and therapy of glaucoma by regulation of homocysteine levels are discussed.
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Mechanisms of the effect of magnesium salts in preeclampsia.
Chiarello, DI, Marín, R, Proverbio, F, Coronado, P, Toledo, F, Salsoso, R, Gutiérrez, J, Sobrevia, L
Placenta. 2018;:134-139
Abstract
Preeclampsia is a heterogeneous pregnancy-specific syndrome associated with abnormal trophoblast invasion and endothelial dysfunction. Magnesium (Mg2+) level may be normal or decreased in women with preeclampsia. However, the use of Mg2+ salts, such as Mg2+ sulphate, are useful in reducing the pathophysiological consequences of preeclampsia with severe features and eclampsia. Although the mechanism of action of this Mg2+ salt is not well understood, the available evidence suggests a beneficial effect of Mg2+ for the mother and foetus. The mechanisms include a lower level of soluble fms-like tyrosine kinase 1 and endoglin, blockage of brain N-methyl-D-aspartate receptors, decreased inflammation mediators, activation of nitric oxide synthases, blockage of arginases, and reduced free radicals level. The maintenance of Mg2+ homeostasis in pregnancy is crucial for an appropriate pregnancy progression. Oral Mg2+ salts can be used for this purpose which could result in mitigating the deleterious consequences of this syndrome to the mother, foetus, and newborn.