Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
Department of Rheumatology, Charlotte Maxeke Johannesburg Academic Hospital, Faculty of Health Sciences, University of the Witwatersrand, South Africa.
Peptides. 2018 Apr;102:31-37. doi: 10.1016/j.peptides.2018.02.002. Epub 2018 Feb 21.
Nesfatin is an anti-inflammatory molecule that reduces atherosclerotic cardiovascular risk. By contrast, visfatin has pro-inflammatory properties and is pro-atherogenic. We examined the potential impact of nesfatin and visfatin on atherosclerotic disease in 232 (113 black and 119 white) consecutive rheumatoid arthritis (RA) patients from 2 centers. Independent relationships of nesfatin and visfatin concentrations with metabolic risk factors, endothelial activation, carotid atherosclerosis and altered plaque stability were determined in multivariable regression models. Rheumatoid factor (RF) positivity was associated with both nesfatin (β = 0.650, p < 0.0001) and visfatin levels (β = 0.157, p = 0.03). Visfatin concentrations were related to increased diastolic blood pressure (β = 4.536, p = 0.01) and diabetes prevalence (β = 0.092, p = 0.04). Nesfatin levels were associated with reduced carotid intima-media thickness (β = -0.017, p = 0.008). Nesfatin (β = 0.116, p = 0.001) and visfatin concentrations (β = 0.234, p = 0.001) were related to those of matrix metalloproteinase-2 (MMP-2), a plaque stability mediator. Nesfatin and visfatin concentrations were directly correlated (Spearman's rho = 0.516). The nesfatin-MMP-2 and visfatin-MMP-2 relations were both stronger in RF negative compared to RF positive patients (interaction p = 0.01 and p = 0.04, respectively). Nesfatin is associated with reduced atherosclerosis and increased plaque stability mediator levels in RA. Visfatin is related to adverse cardio-metabolic risk in RA. Increased MMP-2 expression in relation to visfatin may represent a compensatory mechanism aimed at reducing cardiovascular risk in RA.
内脂素是一种具有抗炎作用的分子，可降低动脉粥样硬化性心血管风险。相比之下，内脏脂肪素具有促炎作用，并促进动脉粥样硬化。我们在来自 2 个中心的 232 例（113 例黑人，119 例白人）连续类风湿关节炎（RA）患者中研究了内脂素和内脏脂肪素对动脉粥样硬化疾病的潜在影响。在多变量回归模型中确定了内脂素和内脏脂肪素浓度与代谢危险因素、内皮激活、颈动脉粥样硬化和斑块稳定性改变之间的独立关系。类风湿因子（RF）阳性与内脂素（β=0.650，p<0.0001）和内脏脂肪素水平（β=0.157，p=0.03）均相关。内脏脂肪素浓度与舒张压升高（β=4.536，p=0.01）和糖尿病患病率（β=0.092，p=0.04）相关。内脂素水平与颈动脉内膜中层厚度降低相关（β=-0.017，p=0.008）。内脂素（β=0.116，p=0.001）和内脏脂肪素浓度（β=0.234，p=0.001）与基质金属蛋白酶-2（MMP-2）相关，MMP-2 是一种斑块稳定性介质。内脂素和内脏脂肪素浓度呈正相关（Spearman 相关系数为 0.516）。在 RF 阴性患者中，内脂素-MMP-2 和内脏脂肪素-MMP-2 关系均强于 RF 阳性患者（交互作用 p=0.01 和 p=0.04）。内脂素与 RA 患者的动脉粥样硬化减少和斑块稳定性介质水平升高相关。内脏脂肪素与 RA 患者的不良心血管代谢风险相关。与内脏脂肪素相关的 MMP-2 表达增加可能代表一种代偿机制，旨在降低 RA 患者的心血管风险。
