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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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Salt Intake and Immunity.
Afsar, B, Kuwabara, M, Ortiz, A, Yerlikaya, A, Siriopol, D, Covic, A, Rodriguez-Iturbe, B, Johnson, RJ, Kanbay, M
Hypertension (Dallas, Tex. : 1979). 2018;(1):19-23
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Endothelial Regenerative Capacity and Aging: Influence of Diet, Exercise and Obesity.
Ross, MD
Current cardiology reviews. 2018;(4):233-244
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Abstract
BACKGROUND The endothelium plays an important role in cardiovascular regulation, from blood flow to platelet aggregation, immune cell infiltration and demargination. A dysfunctional endothelium leads to the onset and progression of Cardiovascular Disease (CVD). The aging endothelium displays significant alterations in function, such as reduced vasomotor functions and reduced angiogenic capabilities. This could be partly due to elevated levels of oxidative stress and reduced endothelial cell turnover. Circulating angiogenic cells, such as Endothelial Progenitor Cells (EPCs) play a significant role in maintaining endothelial health and function, by supporting endothelial cell proliferation, or via incorporation into the vasculature and differentiation into mature endothelial cells. However, these cells are reduced in number and function with age, which may contribute to the elevated CVD risk in this population. However, lifestyle factors, such as exercise, physical activity obesity, and dietary intake of omega-3 polyunsaturated fatty acids, nitrates, and antioxidants, significantly affect the number and function of these circulating angiogenic cells. CONCLUSION This review will discuss the effects of advancing age on endothelial health and vascular regenerative capacity, as well as the influence of diet, exercise, and obesity on these cells, the mechanistic links and the subsequent impact on cardiovascular health.
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New molecular targets of pulmonary vascular remodeling in pulmonary arterial hypertension: importance of endothelial communication.
Guignabert, C, Tu, L, Girerd, B, Ricard, N, Huertas, A, Montani, D, Humbert, M
Chest. 2015;(2):529-537
Abstract
Pulmonary arterial hypertension (PAH) is a disorder in which mechanical obstruction of the pulmonary vascular bed is largely responsible for the rise in mean pulmonary arterial pressure, resulting in a progressive functional decline despite current available therapeutic options. The fundamental pathogenetic mechanisms underlying this disorder include pulmonary vasoconstriction, in situ thrombosis, medial hypertrophy, and intimal proliferation, leading to occlusion of the small to mid-sized pulmonary arterioles and the formation of plexiform lesions. Several predisposing or promoting mechanisms that contribute to excessive pulmonary vascular remodeling in PAH have emerged, such as altered crosstalk between cells within the vascular wall, sustained inflammation and dysimmunity, inhibition of cell death, and excessive activation of signaling pathways, in addition to the impact of systemic hormones, local growth factors, cytokines, transcription factors, and germline mutations. Although the spectrum of therapeutic options for PAH has expanded in the last 20 years, available therapies remain essentially palliative. However, over the past decade, a better understanding of new key regulators of this irreversible pulmonary vascular remodeling has been obtained. This review examines the state-of-the-art potential new targets for innovative research in PAH, focusing on (1) the crosstalk between cells within the pulmonary vascular wall, with particular attention to the role played by dysfunctional endothelial cells; (2) aberrant inflammatory and immune responses; (3) the abnormal extracellular matrix function; and (4) altered BMPRII/KCNK3 signaling systems. A better understanding of novel pathways and therapeutic targets will help in the designing of new and more effective approaches for PAH treatment.
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Effect of a special carbohydrate-protein bar and tomato juice supplementation on oxidative stress markers and vascular endothelial dynamics in ultra-marathon runners.
Samaras, A, Tsarouhas, K, Paschalidis, E, Giamouzis, G, Triposkiadis, F, Tsitsimpikou, C, Becker, AT, Goutzourelas, N, Kouretas, D
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2014;:231-6
Abstract
It is well established that exercise induces excessive production of reactive species leading to oxidative stress, which has been implicated in oxidative damage of macromolecules, immune dysfunction, muscle damage and fatigue. The present study examined the effect of supplementation of ultra-marathon runners for a two-months-period with a special whey protein bar containing carbohydrates and protein in a specific ratio (1:1) (N=16), prepared using as starting material the by-products of cheese manufacturing, and supplementation with commercially available tomato juice (N=15). Thiobarbituric-acid reactive substances and protein carbonyls were significantly decreased in both supplementation groups, while a pronounced increased in reduced glutathione was observed in the protein bar group. Total anti-oxidant activity remained unchanged in both groups. Flow-mediated dilatation, used as an estimate of endothelial function, was increased in both groups, with a significant rise observed only in the tomato juice administration group. In conclusion, supplementation of ultra marathon runners for a two-months-period with a special protein bar and tomato juice significantly improved the oxidative status of the subjects, while tomato juice also improved vascular endothelial function in these athletes.