Taylor Erin B, Ryan Michael J
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA.
Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA
Ther Adv Cardiovasc Dis. 2016 Mar 15;11(1):20-32. doi: 10.1177/1753944716637807.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that predominately affects women of reproductive age. Hypertension is an important cardiovascular risk factor that is prevalent in this patient population. Despite the high incidence of hypertension in women with SLE, the pathophysiological mechanisms underlying the development of hypertension remain poorly understood. This review will focus on disease-related factors, including inflammation, autoantibodies, and sex hormones that may contribute to hypertension in patients with SLE. In addition, we will highlight studies performed by our laboratory using the female NZBWF1 (F1 hybrid of New Zealand Black and New Zealand White strains) mouse model, a spontaneous model of SLE that mimics human disease and develops hypertension and renal injury. Specifically, using female NZBWF1 mice, we have demonstrated that multiple factors contribute to the pathogenesis of hypertension, including the inflammatory cytokine, tumor necrosis factor (TNF)-α, oxidative stress, as well as B-cell hyperactivity and autoantibody production.
系统性红斑狼疮(SLE)是一种慢性自身免疫性疾病,主要影响育龄女性。高血压是一种重要的心血管危险因素,在该患者群体中很常见。尽管SLE女性患者中高血压的发病率很高,但其发生高血压的病理生理机制仍知之甚少。本综述将聚焦于与疾病相关的因素,包括炎症、自身抗体和性激素,这些因素可能导致SLE患者发生高血压。此外,我们将重点介绍我们实验室使用雌性NZBWF1(新西兰黑鼠和新西兰白鼠品系的F1杂交种)小鼠模型所进行的研究,该模型是一种SLE自发模型,可模拟人类疾病并发生高血压和肾损伤。具体而言,使用雌性NZBWF1小鼠,我们已经证明多种因素促成了高血压的发病机制,包括炎性细胞因子、肿瘤坏死因子(TNF)-α、氧化应激,以及B细胞功能亢进和自身抗体产生。