Plasma visfatin levels are associated with major adverse cardiovascular events in patients with acute ST-elevation myocardial infarction

Hung, Wei‐Chin; Yu, Teng‐Hung; Hsu, Chia‐Chang; Liu, Lu; Chung, Fu‐Mei; Tsai, I‐Ting; Lu, Yung‐Chuan; Houng, Jer-Yiing; Lee, Yau-Jiunn; Wang, Chao-Ping

doi:10.25011/cim.v38i3.22705

Cited by 20 publications

(17 citation statements)

References 34 publications

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“…*p < 0.05 vs respective basal values in the absence of visfatin/eNampt. 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] .…”

Section: Figurementioning

confidence: 95%

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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Section: Figurementioning

confidence: 95%

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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“…Levels of plasma triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol, uric acid, creatinine, and glucose were determined by standard commercial methods using a parallel-multichannel analyzer (Hitachi 7170A, Tokyo, Japan), as described previously [11]. Levels of plasma C-reactive protein (CRP) were measured using a high-sensitivity method (IMMAGE; Beckman Coulter, Immunochemistry Systems, Brea, CA) with a detection limit of 0.2 mg/L.…”

Section: Methodsmentioning

confidence: 99%

The burden of major adverse cardiac events in patients with coronary artery disease

Tsai

Wang

et al. 2017

BMC Cardiovasc Disord

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124

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BackgroundPatients with a history of cardiovascular disease are at high risk of developing secondary major adverse cardiac events (MACE). This study aimed to identify independent predictors of MACE after hospital admission which could be used to identify of high-risk patients who may benefit from preventive strategies.MethodsThis study included 1,520 consecutive patients with coronary artery disease (CAD) (654 with acute coronary syndrome (ACS) and 866 with elective percutaneous coronary intervention (PCI) patients) who received PCI and/or stenting. MACE was defined as all-cause mortality or rehospitalization for a cardiovascular- related illness. Cardiovascular-related illnesses included heart failure, reinfarction (nonfatal), recurrence of angina pectoris and repeat PCI or coronary artery bypass graft.ResultsDuring a mean follow-up period of 32 months, 558 of the 1,520 patients developed at least one MACE. Cox regression analysis showed that the baseline clinical and biochemical variables which associated with MACE were age, being illiterate, a widow or widower, and/or economically dependent, having triple vessel disease, stent implantation, anemia, and/or diabetes mellitus, waist to hip ratio (WHR), diastolic blood pressure, fasting glucose, total cholesterol, high-density lipoprotein cholesterol (HDL-C), creatinine, estimated glomerular filtration rate (eGFR), red blood cell count, hemoglobin, hematocrit, and mean corpuscular-hemoglobin concentration (MCHC) in ACS patients, and age, malnourished, and/or economically dependent, taking hypoglycemic medication, having triple vessel disease, stent implantation, anemia, diabetes mellitus, and/or hypertension, WHR, fasting glucose, HDL-C, uric acid, creatinine, eGFR, high-sensitivity C-reactive protein, mean corpuscular volume, and MCHC in elective PCI patients. Using multivariate Cox regression analysis, we found the MACE’s independent factors are triple vessel disease, stent implantation, hypertension, and eGFR in ACS patients, and having triple vessel disease, stent implantation, hypertension, and uric acid in elective PCI patients.ConclusionsHaving triple vessel disease, stent implantation, hypertension, and eGFR or uric acid independently predicted MACE in patients with CAD after long-term follow-up. Fortunately, these factors are modifiable and should be identified and monitored early.

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“…[45][46][47] In addition, blood NAMPT levels are higher under retinal ischemia 48 and intestinal ischemia. 49 However, such results are anticipated since NAMPT is a stress sensor, and these results cannot answer whether NAMPT is a friend or foe of the ischemic injury and the postischemic vascular repair.…”

Section: Nampt and Nampt-controlled Nad Pool In Ischemic Diseases Andmentioning

confidence: 99%

NAMPT and NAMPT-controlled NAD Metabolism in Vascular Repair

Wang

Liu

et al. 2016

Journal of Cardiovascular Pharmacology

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Vascular repair plays important roles in postischemic remodeling and rehabilitation in cardiovascular and cerebrovascular disease, such as stroke and myocardial infarction. Nicotinamide adenine dinucleotide (NAD), a well-known coenzyme involved in electron transport chain for generation of adenosine triphosphate, has emerged as an important controller regulating various biological signaling pathways. Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for NAD biosynthesis in mammals. NAMPT may also act in a nonenzymatic manner, presumably mediated by unknown receptor(s). Rapidly accumulating data in the past decade show that NAMPT and NAMPT-controlled NAD metabolism regulate fundamental biological functions in endothelial cells, vascular smooth muscle cells, and endothelial progenitor cells. The NAD-consuming proteins, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38, may contribute to the regulatory effects of NAMPT-NAD axis in these cells and vascular repair. This review discusses the current data regarding NAMPT and NAMPT-controlled NAD metabolism in vascular repair and the clinical potential translational application of NAMPT-related products in treatment of cardiovascular and cerebrovascular disease.

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Plasma visfatin levels are associated with major adverse cardiovascular events in patients with acute ST-elevation myocardial infarction

Cited by 20 publications

References 34 publications

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

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

The burden of major adverse cardiac events in patients with coronary artery disease

NAMPT and NAMPT-controlled NAD Metabolism in Vascular Repair

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