Vitamin D Deficiency and Cardiovascular Diseases

2020 ◽  
Vol 12 (1) ◽  
pp. 27-37
Author(s):  
Yifei Wang ◽  
Shi Zhou ◽  
Shuai Lei ◽  
Liying Hao ◽  
Deri Sun ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cardiovascular Diseases ◽  
Vitamin D Deficiency ◽  
Cardiovascular Events ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Hormone Effects ◽  
Peptide Expression ◽  
Novel Strategy ◽  
Underlying Mechanisms

In recent years, there are increasing evidences of epidemiology and clinic which indicate that vitamin D deficiency has relationship with cardiovascular disease. It was found the levels of vitamin D were negatively correlated with cardiovascular events such as hypertension, heart failure, atrial fibrillation and coronary heart disease. This article reviews the connection between cardiovascular diseases and vitamin D, and explains the underlying mechanisms including regulating renin-angiotensin system or endothelial function, inhibition of natriuretic peptide expression or the release of parathyroid hormone, effects on inflammation or obesity, bioenergetics, activation of extracellular Ca2+, inhibition of oxidative stress, and so on. These mechanisms provide novel strategy for the treatment of these cardiovascular diseases.

scholarly journals Vitamin D Deficiency Aggravates Nephrotoxicity, Hypertension and Dyslipidemia Caused by Tenofovir: Role of Oxidative Stress and Renin-Angiotensin System

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e103055 ◽  
Author(s):  
Daniele Canale ◽  
Ana Carolina de Bragança ◽  
Janaína Garcia Gonçalves ◽  
Maria Heloisa Massola Shimizu ◽  
Talita Rojas Sanches ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Chronic vitamin D deficiency induces lung fibrosis through activation of the renin-angiotensin system

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Yongyan Shi ◽  
Tianjing Liu ◽  
Li Yao ◽  
Yujiao Xing ◽  
Xinyi Zhao ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Lung Fibrosis ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Vitamin D deficiency in critically ill patients diagnosed with COVID -19. Are we doing enough? A retrospective analysis of 226 patients.

2020 ◽  
Author(s):  
Tomás Cuñat ◽  
Antonio Ojeda ◽  
Andrea Calvo
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Distress Syndrome ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Hydroxyvitamin D ◽  
Vitamin D Levels ◽  
25 Hydroxyvitamin D

Abstract Vitamin D deficiency is common in critically ill patients, and its role in COVID-19 patients could be important. Its deficiency has been associated with respiratory distress syndrome, pulmonary fibrosis (through activation of the renin-angiotensin system), increased levels of IL-2, and cardiovascular adverse events. Various scientific societies recommend the screening of vitamin D in individuals at risk for deficiency. Despite that, the demographics of Vitamin D levels amongst critically ill patients with a confirmed diagnosis of COVID-19 are currently unknown. We propose a study to determine the prevalence of vitamin D deficiency in a consecutive population of COVID-19 patients admitted to intensive care units and to evaluate its relationship with clinical outcomes. We study 226 COVID-19 patients between March 16 and April 26, 2020. The prevalence of vitamin D deficiency could not be determined because the value of 25-hydroxyvitamin D was obtained in a few patients (17 patients, 7,5%). However, all patients with serum determinations of 25-hydroxyvitamin D presented a level lower than 20 ng/ml and thirteen patients (76,5%) levels < 12,5 ng/ml. We conclude that undiagnosed vitamin D deficiency is common in critically ill COVID-19 patients, and physicians should be conscious of the relevance of its monitoring and supplementation.

scholarly journals Vitamin D suppresses bleomycin-induced pulmonary fibrosis by targeting the local renin–angiotensin system in the lung

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jianjun Chang ◽  
Hongguang Nie ◽  
Xin Ge ◽  
Jie Du ◽  
Weicheng Liu ◽  
...  
Keyword(s):  
Vitamin D ◽  
Weight Loss ◽  
Angiotensin Ii ◽  
Vitamin D Deficiency ◽  
Lung Fibrosis ◽  
Collagen Type ◽  
Renin Angiotensin System ◽  
Collagen Type I ◽  
Type I ◽  
Angiotensin System

AbstractIdiopathic pulmonary fibrosis (IPF) is a severe disorder leading to progressive and irreversible loss of pulmonary function. In this study we investigated the anti-fibrotic effect of vitamin D using a mouse model of IPF. Lung fibrosis was induced with bleomycin in vitamin D-sufficient and vitamin D-deficient C57BL/6 mice. We found that treatment with active vitamin D analog paricalcitol prevented mouse body weight loss and alleviated lung fibrosis, whereas vitamin D deficiency severely aggravated lung injury. At the molecular level, paricalcitol treatment suppressed the induction of fibrotic inducer TGF-β and extracellular matrix proteins α-SMA, collagen type I and fibronectin in the lung, whereas vitamin D deficiency exacerbated the induction of these proteins. Interestingly, bleomycin treatment activated the local renin–angiotensin system (RAS) in the lung, manifested by the induction of renin, angiotensinogen, angiotensin II and angiotensin receptor type 1 (AT1R). Paricalcitol treatment suppressed the induction of these RAS components, whereas vitamin D deficiency enhanced the activation of the lung RAS. We also showed that treatment of bleomycin-induced vitamin D-deficient mice with AT1R antagonist losartan relieved weight loss, substantially ameliorated lung fibrosis and markedly blocked TGF-β induction in the lung. Moreover, we demonstrated that in lung fibroblast cultures, TGF-β and angiotensin II synergistically induced TGF-β, AT1R, α-SMA, collagen type I and fibronectin, whereas 1,25-dihydroxyvitamin D markedly suppressed the induction of these fibrotic markers. Collectively, these observations strongly suggest that vitamin D mitigates lung fibrosis by blocking the activation of the lung RAS in this mouse model of IPF.

The Renin Angiotensin System and Bipolar Disorder: A Systematic Review

2020 ◽  
Vol 27 (6) ◽  
pp. 520-528 ◽  
Author(s):  
Izabela Guimarães Barbosa ◽  
Giulia Campos Ferreira ◽  
Diomildo Ferreira Andrade Júnior ◽  
Cássio Rocha Januário ◽  
André Rolim Belisário ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bipolar Disorder ◽  
Cardiovascular Diseases ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Receptors ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Search Terms

Bipolar Disorder (BD) is a chronic a multifactorial psychiatric illness that affects mood, cognition, and functioning. BD is associated with several psychiatric conditions as well clinical comorbidities, particularly cardiovascular diseases. The neurobiology of BD is complex and multifactorial and several systems have been implicated. Considering that the Renin Angiotensin System (RAS) plays an important role in cardiovascular diseases and that recently evidence has suggested its role in psychiatric disorders, the aim of the present study is to summarize and to discuss recent findings related to the modulation of RAS components in BD. A systematic search of the literature using the electronic databases MEDLINE and LILACS was conducted through March 2019. The search terms were: “Bipolar Disorder”; “Renin Angiotensin System”; “Angiotensin 2”; “Angiotensin receptors”; “Angiotensin 1-7”; “ACE”; “ACE2”; “Mas Receptor”. We included original studies assessing RAS in BD patients. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. In the majority of studies (6 of 8), the ACE insertion/deletion (I/D) polymorphism did not differ between BD patients and controls. BD patients presented higher plasma renin activity in comparison with controls. The studies evaluating the RAS molecules in BD are very scarce and heterogeneous. The literature suggests a potential role of RAS in BD. Further studies are necessary to investigate this relationship.

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