2016
DOI: 10.1161/atvbaha.116.307530
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

Abstract: VDR activation reduces dissecting AAA formation induced by Ang-II in apoE(-/-) mice and may constitute a novel therapeutic strategy to prevent AAA progression.

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Cited by 61 publications
(50 citation statements)
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“…Doses for lixisenatide and liraglutide were chosen based on the previously reported optimal doses obtained from pharmacokinetic and drug-clearance studies in rodents described for lixisenatide [11,15,16] and liraglutide [12,[17][18][19]. Blood pressure was measured in conscious mice using a non-invasive tail-cuff system (LE5002 Pressure Meter; Panlab, Barcelona, Spain) as previously described [20].…”
Section: Methodsmentioning
confidence: 99%
“…Doses for lixisenatide and liraglutide were chosen based on the previously reported optimal doses obtained from pharmacokinetic and drug-clearance studies in rodents described for lixisenatide [11,15,16] and liraglutide [12,[17][18][19]. Blood pressure was measured in conscious mice using a non-invasive tail-cuff system (LE5002 Pressure Meter; Panlab, Barcelona, Spain) as previously described [20].…”
Section: Methodsmentioning
confidence: 99%
“…Mice with endothelial-specific deletion of the VDR exhibit reduced eNOS expression, impaired endotheliumdependent vasorelaxation, and an augmented pressor effect of angiotensin II [137]. Furthermore, vitamin D can exert powerful immunomodulatory actions to modify the immune response to injury during various diseases, including atherosclerosis [64,138], cancer [25], asthma [139], and stroke [50]. In particular, vitamin D can attenuate inflammatory responses and promote protein homeostasis via modulating the NF-κB and unfolded protein response (UPR) pathways, respectively [140,141].…”
Section: Vitamin D Deficiency and Its Impact On Cerebrovascular Diseasesmentioning
confidence: 99%
“…Reduction in AAA dissection, induced by Angiotensin-II in apoE −/− mice, by VDR activation with oral vitamin D suggests the potential therapeutic role of vitamin D to decrease the AAA progression [115]. The reduction in the progression of AAA was attributed to decrease in many parameters, including macrophage infiltration, neo-vessel formation, MMP-2 and MMP-9 activation, chemokines (CCL2, CCL5, CXCL1) expression, and extracellular signal–regulated kinases 1/2, p38 mitogen-activated protein kinase, and NF-κB activity (Figure 3).…”
Section: Vascular Diseasementioning
confidence: 99%