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铁与缺氧及细胞代谢的交叉点。对肺动脉高压病理生物学的影响。

The crossroads of iron with hypoxia and cellular metabolism. Implications in the pathobiology of pulmonary hypertension.

作者信息

Robinson Jeffrey C, Graham Brian B, Rouault Tracey C, Tuder Rubin M

机构信息

1 Program in Translational Lung Research, Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado; and.

出版信息

Am J Respir Cell Mol Biol. 2014 Dec;51(6):721-9. doi: 10.1165/rcmb.2014-0021TR.

DOI:10.1165/rcmb.2014-0021TR
PMID:24988529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4291546/
Abstract

The pathologic hallmark of pulmonary arterial hypertension (PAH) is pulmonary vascular remodeling, characterized by endothelial cell proliferation, smooth muscle hypertrophy, and perivascular inflammation, ultimately contributing to increased pulmonary arterial pressures. Several recent studies have observed that iron deficiency in patients with various forms of PAH is associated with worsened clinical outcome. Iron plays a key role in many cellular processes regulating the response to hypoxia, oxidative stress, cellular proliferation, and cell metabolism. Given the potential importance of iron supplementation in patients with the disease and the broad cellular functions of iron, we review its role in processes that pertain to PAH.

摘要

肺动脉高压(PAH)的病理标志是肺血管重塑,其特征为内皮细胞增殖、平滑肌肥大和血管周围炎症,最终导致肺动脉压力升高。最近的几项研究观察到,各种形式PAH患者的缺铁与临床结局恶化有关。铁在调节对缺氧、氧化应激、细胞增殖和细胞代谢反应的许多细胞过程中起关键作用。鉴于补充铁对该病患者的潜在重要性以及铁广泛的细胞功能,我们综述其在与PAH相关过程中的作用。

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本文引用的文献

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Iron deficiency in systemic sclerosis patients with and without pulmonary hypertension.系统性硬化症患者合并与不合并肺动脉高压时的缺铁情况。
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