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- W2114157036 abstract "See related article, pp 158–166 Accumulating evidence indicates that aldosterone plays a predominant role in the pathobiology of cardiopulmonary vascular fibrosis. Mineralocorticoid receptor activation disrupts normal vessel architecture by promoting collagen and elastin degradation, as well as deposition of newly synthesized collagen, which has attendant consequences for both vascular structure and function. The clinical relevance of this concept is supported by epidemiological studies that have shown that vascular stiffness occurs before hypertension and link increased serum aldosterone levels to incident hypertension.1,2 Further support for this concept is found in selected patient populations, including patients with primary aldosteronism, congestive heart failure, and obesity, where evidence of mineralocorticoid receptor activation is associated with circulating markers of fibrosis and increased collagen turnover.3–5 Although these studies provide a framework to explore the association between aldosterone and fibrosis, arterial stiffness, and hypertension, they do not inform on the critical molecular mechanisms or relevant signaling pathways that initiate collagen synthesis and ultimately lead to vascular fibrosis.In this issue of Hypertension, Tarjus et al6 provide compelling evidence that neutrophil gelatinase–associated lipocalin (NGAL), or lipocalin-2 (Lcn2), is a key mediator of mineralocorticoid-stimulated vascular fibrosis. They convincingly show that NGAL/Lcn2 is associated with aldosterone levels and markers of collagen metabolism in nonhypertensive asymptomatic individuals with abdominal obesity. The authors also provide mechanistic insight to support the central role of Lcn2 by conducting studies in Lcn2 conditional knockout mice using the uninephrectomy/aldosterone infusion/salt model. Under these conditions, absence of Lcn2 expression is associated with lower blood …" @default.
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- W2114157036 date "2015-07-01" @default.
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- W2114157036 title "The Central Role of Neutrophil Gelatinase–Associated Lipocalin in Cardiovascular Fibrosis" @default.
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- W2114157036 doi "https://doi.org/10.1161/hypertensionaha.115.05479" @default.
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