2017
DOI: 10.1016/j.clinre.2017.01.005
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Evaluation of endothelial dysfunction in patients with nonalcoholic fatty liver disease: Association of selenoprotein P with carotid intima-media thickness and endothelium-dependent vasodilation

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Cited by 28 publications
(27 citation statements)
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“…SEPP levels were also shown to be inversely associated with MetS [19,24]. These and our findings are contradictory to other 2 studies showing higher SEPP in NAFLD patients than controls [17,18]. However, in these studies, BMI and/or WC were lower in the controls than NAFLD patients, and the NAFLD diagnosis was based on computerized tomography [17] or ultrasound [18].…”
Section: Discussioncontrasting
confidence: 99%
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“…SEPP levels were also shown to be inversely associated with MetS [19,24]. These and our findings are contradictory to other 2 studies showing higher SEPP in NAFLD patients than controls [17,18]. However, in these studies, BMI and/or WC were lower in the controls than NAFLD patients, and the NAFLD diagnosis was based on computerized tomography [17] or ultrasound [18].…”
Section: Discussioncontrasting
confidence: 99%
“…These and our findings are contradictory to other 2 studies showing higher SEPP in NAFLD patients than controls [17,18]. However, in these studies, BMI and/or WC were lower in the controls than NAFLD patients, and the NAFLD diagnosis was based on computerized tomography [17] or ultrasound [18]. In the latter study, SEPP was ▶table 1 Unadjusted and adjusted comparative data between patients with SS, borderline and definite NASH, and controls.…”
Section: Discussioncontrasting
confidence: 99%
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“…TGFβ, PDGF and FGF), and hypoxia-induced vasomotion and vesicular remodeling. 60) Using PAH patient-derived lung tissue and pulmonary artery smooth muscle cells (PASMCs), as well as Selenop −/− mice, Kikuchi and coworkers showed that 1) plasma SeP in PAH patients was elevated likely due to SeP overexpression in PASMCs, but not in the liver; 2) PAH-PASMCs secrete and receive SeP, as an autocrine signal, to promote their own proliferation and survival by activating the AKT, extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinase (MAPK) and HIF1α pathways, probably through ApoER2; 3) SeP is induced in mice when exposed to hypoxia (10% O 2 ) that causes the muscularization of pulmonary arteries and pulmonary hypertension, mimicking human PAH; and, 4) Selenop −/− mice were resistant to the induction of PAH-related symptoms by hypoxia compared to wild-type animals, whereas the exogenous expression of SeP in wild-type mice exacerbates the symptoms. 21) Together, these demonstrated an essential role of SeP in PAH progression, suggesting SeP as a therapeutic target for this heretofore undruggable disease.…”
Section: Pah and Sepmentioning
confidence: 99%