Plasma visfatin/nicotinamide phosphoribosyltransferase levels in hypertensive elderly – results from the PolSenior substudy

Kocełak, Piotr; Olszanecka-Glinianowicz, Magdalena; Owczarek, Aleksander; Bożentowicz-Wikarek, Maria; Brzozowska, Aniceta; Mossakowska, Małgorzata; Zdrojewski, Tomasz; Grodzicki, Tomasz; Wiȩcek, Andrzej; Chudek, Jerzy

doi:10.1016/j.jash.2014.11.002

Cited by 18 publications

(12 citation statements)

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“…In agreement with the observation in elderly patients, 52 plasma visfatin concentrations did not correlate with blood pressure but correlated with the degree of insulin resistance. Contrary to the observation by Lan et al, 53 we observed no significant changes in plasma visfatin concentrations after treatment with ARB and amlodipine.…”

supporting

confidence: 90%

Effects of antihypertensive treatment on plasma apelin, resistin, and visfatin concentrations

Skoczylas¹,

Piecha²,

Wiȩcek³

2016

Polish Archives of Internal Medicine

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supporting

confidence: 90%

Effects of antihypertensive treatment on plasma apelin, resistin, and visfatin concentrations

Skoczylas¹,

Piecha²,

Wiȩcek³

2016

Polish Archives of Internal Medicine

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“…In our own analysis, after dividing the patients into those suffering from arterial hypertension and those without the disease, there was no statistically significant difference in visfatin concentration between these subgroups (p = 0.749). Similar results were presented by Kocelak et al 37 from a study on a large group of 2,789 older Polish patients. The authors divided the patients into groups composed of people without hypertension, patients with pharmacologically regulated hypertension and those untreated for the disease.…”

Section: Discussionsupporting

confidence: 90%

Assessment of visfatin concentrations in the serum of male psoriatic patients in relation to metabolic abnormalities

et al. 2020

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“…Indeed, the link between visfatin/eNampt and cardiovascular diseases has been even reinforced by more recent reports 28,29 , both in the presence or in the absence or metabolic alterations 19,30,31 . A common ground of clinical studies linking visfatin/eNampt with cardiovascular diseases highlights the clear relationship between this adipokine and a pro-inflammatory context [32][33][34] . Moreover, there is a meta-analysis suggesting that visfatin/ eNampt may be a promising biomarker not only for predicting obesity, diabetes status, insulin resistance, or metabolic syndrome but also for the development of cardiovascular disease 35 .…”

Section: Figurementioning

confidence: 99%

Visfatin/eNampt induces endothelial dysfunction in vivo: a role for Toll-Like Receptor 4 and NLRP3 inflammasome

Romacho

Valencia

Ramos-González

et al. 2020

Sci Rep

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Visfatin/extracellular-nicotinamide-phosphoribosyltranferase-(enampt) is a multifaceted adipokine enhanced in type-2-diabetes and obesity. Visfatin/eNampt cause in vitro endothelial dysfunction and vascular inflammation, although whether the same effects are achieved in vivo is unknown. Toll-like receptor-4 (TLR4), a main surface pattern recognition receptor of innate immune system is a potential target for visfatin/eNampt. We studied its capacity to generate vascular dysfunction in vivo, focusing on TLR4 role and downstream activation of nod-like-receptor-protein-3 (NLRP3)-inflammasome. 4 month-old C57BL/6 mice were exposed to 7 days infusion of visfatin/eNampt, alone or together with FK 866 (Nampt enzymatic inhibitor), CLI 095 (TLR4 blocker), MCC 950 (NLRP3-inflammasome inhibitor), or anakinra (interleukin(IL)-1-receptor antagonist). Endothelial dysfunction was tested in isolated microvessels. In human umbilical endothelial cells (HUVEC), proteins related to the NLRP3inflammasome phosphorylated p-65, NLRP3, caspase-1, pro-IL-1β, and mature IL-1β were determined by Western blot, while the inflammasome related apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC-specks) was studied by immunofluorescence. Impaired endotheliumdependent relaxations were observed in isolated mesenteric microvessels from visfatin/eNamptinfused mice. This effect was attenuated by co-treatment with FK 866 or CLI 095, supporting a role for Nampt enzymatic activity and TLR4 activation. Moreover, cultured HUVEC exposed to visfatin/ eNampt showed higher expression and activation of NLRP3-inflammasome. Again, this effect relied on Nampt enzymatic activity and TLR4 activation, and it was abrogated by the inflammasome assembly blockade with MCC 950. The endothelial dysfunction evoked by visfatin/eNampt infusion in vivo was also sensitive to both MCC 950 and anakinra treatments, suggesting that the NLRP3-inflammasomedriven tissular release of IL-1β is the final mediator of endothelial damage. We conclude that Visfatin/ enampt produces in vivo vascular dysfunction in mice by a Nampt-dependent TLR4-mediated pathway, involving NLRP3-inflammasome and paracrine IL-1β. Thus, those targets may become therapeutic strategies for attenuating the adipokine-mediated vascular dysfunction associated to obesity and/or type-2-diabetes.

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Plasma visfatin/nicotinamide phosphoribosyltransferase levels in hypertensive elderly – results from the PolSenior substudy

Cited by 18 publications

References 50 publications

Effects of antihypertensive treatment on plasma apelin, resistin, and visfatin concentrations

Effects of antihypertensive treatment on plasma apelin, resistin, and visfatin concentrations

Assessment of visfatin concentrations in the serum of male psoriatic patients in relation to metabolic abnormalities

Visfatin/eNampt induces endothelial dysfunction in vivo: a role for Toll-Like Receptor 4 and NLRP3 inflammasome

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