一氧化氮、氧化应激与肺动脉高压中的炎症反应
Nitric oxide, oxidative stress and inflammation in pulmonary arterial hypertension.
机构信息
Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73126-0901, USA.
出版信息
J Hypertens. 2010 Feb;28(2):201-12. doi: 10.1097/HJH.0b013e328332bcdb.
Abstract
Pulmonary arterial hypertension (PAH) is a chronic and progressive disease characterized by a persistent elevation of pulmonary artery pressure accompanied by right ventricular hypertrophy (RVH). The current treatment for pulmonary hypertension is limited and only provides symptomatic relief due to unknown cause and pathogenesis of the disease. Both vasoconstriction and structural remodeling (enhanced proliferation of vascular smooth muscle cell) of the pulmonary arteries contribute to the progressive course of PAH, irrespective of different underlying causes. The exact molecular mechanism of PAH, however, is not fully understood. The purpose of this review is to provide recent advances in the mechanistic investigation of PAH. Specifically, this review focuses on nitric oxide, oxidative stress and inflammation and how these factors contribute to the development and progression of PAH. This review also discusses recent and potential therapeutic advancements for the treatment of PAH.
摘要
肺动脉高压（PAH）是一种慢性进行性疾病，其特征是肺动脉压持续升高，并伴有右心室肥厚（RVH）。目前对肺动脉高压的治疗有限，由于对疾病的病因和发病机制尚不清楚，仅能提供对症缓解。肺动脉的血管收缩和结构重塑（血管平滑肌细胞的过度增殖）都导致 PAH 的进行性发展，而与不同的潜在病因无关。然而，PAH 的确切分子机制尚未完全阐明。本综述的目的是提供 PAH 的机制研究的最新进展。具体来说，本综述侧重于一氧化氮、氧化应激和炎症，以及这些因素如何导致 PAH 的发生和发展。本综述还讨论了治疗 PAH 的最新和潜在治疗进展。
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