Coronary artery embryogenesis in cardiac defects induced by retinoic acid in mice

Ratajska, Anna; Złotorowicz, Renata; Błażejczyk, Magdalena; Wasiutyński, Aleksander

doi:10.1002/bdra.20200

Cited by 18 publications

(20 citation statements)

References 48 publications

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“…Interestingly, CAs do not connect with the pulmonary artery under these conditions, even in the presence of dramatic morphological defects. Similar phenotypes have been observed in Cx43-, Tbx1-, and perlecan-null mice (18)(19)(20) as well as in retinoic acid-treated embryos (21). Coronary stems are also abnormal in human hearts with rotation defects called Coronary arteries (CAs) stem from the aorta at 2 highly stereotyped locations, deviations from which can cause myocardial ischemia and death.…”

Section: Introductionsupporting

confidence: 54%

VEGF-C and aortic cardiomyocytes guide coronary artery stem development

et al. 2014

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Section: Introductionsupporting

confidence: 54%

VEGF-C and aortic cardiomyocytes guide coronary artery stem development

et al. 2014

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“…[8][9][10] An excess or deficiency of vitamin A or its derivative RA may cause various cardiac malformations. 11,12 The all-trans RA has been shown to modulate proliferative ability and promote reendothelialization after arterial injury. 13 In addition, RA treatment prevented adverse cardiac remodeling through inhibition of the expression of renin-angiotensin system components in hypertensive rodents.…”

mentioning

confidence: 99%

Association of Serum Retinoic Acid With Risk of Mortality in Patients With Coronary Artery Disease

Liu

Chen

et al. 2016

Circulation Research

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In multivariate analyses, the hazard ratios for total mortality among those in the lowest (referent) to highest quartiles of serum RA measured at study entry were 1.0, 0.83, 0.74, and 0.56, respectively (P-trend<0.001). For cardiovascular mortality, the comparable hazard ratios were 1.0, 0.76, 0.69, and 0.60 (P-trend<0.001). Furthermore, high RA levels (defined as >median) were associated with lower risk of total mortality (adjusted hazard ratios, 0.68; 95% confidence interval, 0.50-0.85; P=0.001) and cardiovascular mortality (adjusted hazard ratios, 0.62; 95% confidence interval, 0.45-0.78; P<0.001) compared with low RA (defined as ≤median). rodents. 14 Furthermore, all-trans RA treatment was shown to be effective in restoring the cardioprotective oxytocin-natriuretic peptides system and preventing abnormal cardiac remodeling in the ob/ob mice. 15 Our recent study showed that dietary supplementation of RA attenuated the development of atherosclerotic lesions in apolipoprotein E-deficient mice. 16 The improved effects of RA on cardiovascular diseases were further demonstrated in the in vitro studies that are involved in different types of cardiovascular cells. Activation of retinoid signaling effectively enhanced cholesterol efflux from cholesterol-loaded macrophage foam cells. [16][17][18] RA treatment inhibited the secretion of coagulatory factors from endothelial cells under proinflammatory conditions. Conclusions19 Thus, retinoid therapy may have important implications in limiting or regressing atherosclerotic cardiovascular disease.Although animal studies provided the appealing data that RA supplementation might be a promising therapeutic nutrient for cardiovascular disease, the clinical relevance of circulating RA in the cardiovascular disease have not been carefully investigated before. Therefore, in this study, we prospectively evaluated the relationship of serum RA with the risk of mortality in patients with coronary artery disease (CAD). Methods Study SubjectsStudy participants were recruited between October 2008 and December 2011 as part of the Expanded Guangdong Coronary Artery Disease Cohort (EGCADC).20-23 EGCADC consisted of patients aged from 40 to 80 years old recruited from GCADC and outpatients from Guangdong General Hospital following the same inclusion and exclusion criteria, ascertainment of CAD, questionnaires and study protocol. A total of 2523 CAD patients were included in the EGCADC (1513 from GCADC and another 1010 from Guangdong General Hospital). The patients will be enrolled if they met one of the following inclusion criteria: history of myocardial infarction (MI), angiographic evidence of >50% stenosis in ≥1 coronary vessels, evidence of exercise-induced ischemia by treadmill or nuclear testing, and history of coronary revascularization or documented diagnosis of CAD by an internist or cardiologist. Participants were excluded if they could not walk 1 block, had MI within the past 6 months, malignancy, with missing or incomplete angiographic data, missing blood samples, laboratory me...

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“…In cases such as Bland-WhiteGarland syndrome, this signal is imprecise allowing the primordia to grow towards the pulmonary trunk (1933). In congenital heart malformations, however, with dextroposition of the aorta relative to the pulmonary trunk, the primordial coronary arteries grow towards the aorta (Gonzáles-Iriarte et al, 2003;Ratajska et al, 2005).…”

Section: B Amentioning

confidence: 99%