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慢性阻塞性肺疾病相关血管重塑中的活性氧物种

Reactive Oxygen Species in COPD-Related Vascular Remodeling.

作者信息

Zuo Li, Chuang Chia-Chen, Clark Alexander D, Garrison Davis E, Kuhlman Jamie L, Sypert David C

机构信息

Molecular Physiology and Rehabilitation Research Laboratory, Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, 43210, USA.

出版信息

Adv Exp Med Biol. 2017;967:399-411. doi: 10.1007/978-3-319-63245-2_26.

Abstract

The pathogenesis of chronic obstructive pulmonary disease (COPD) is a multifaceted process involving the alteration of pulmonary vasculature. Such vascular remodeling can be associated with inflammation, shear stress, and hypoxia-conditions commonly seen in patients with lung diseases. Particularly, the overproduction of reactive oxygen species (ROS) in the diseased lungs contributes greatly to pulmonary vascular remodeling. ROS play an important role in vascular homeostasis, yet excessive ROS can alter pulmonary vasculature and impair lung function, as implicated in COPD at all stages. Increased inflammatory cell infiltration and endothelial dysfunction both correspond to the severity of COPD. As a byproduct of vascular remodeling, pulmonary hypertension negatively affects the long-term survival rate of COPD patients. While there is currently no cure for COPD, several treatment options have focused on alleviating COPD symptoms. Interventions such as long-term oxygen therapy, endothelium-targeted treatment, and pharmacological therapies show promising results in improving the life span of COPD patients and attenuating the progression of pulmonary hypertension. In this chapter, we aim to discuss the contributing factors of pulmonary vascular remodeling in COPD with an emphasis on the ROS, as well as potential redox treatments for COPD-related vascular remodeling.

摘要

慢性阻塞性肺疾病(COPD)的发病机制是一个涉及肺血管系统改变的多方面过程。这种血管重塑可能与炎症、剪切应力以及肺部疾病患者常见的缺氧状况有关。特别是,患病肺部中活性氧(ROS)的过度产生在很大程度上促成了肺血管重塑。ROS在血管稳态中发挥重要作用,但过量的ROS会改变肺血管系统并损害肺功能,这在COPD的各个阶段都有体现。炎症细胞浸润增加和内皮功能障碍均与COPD的严重程度相关。作为血管重塑的一个副产品,肺动脉高压对COPD患者的长期生存率产生负面影响。虽然目前COPD无法治愈,但有几种治疗选择致力于缓解COPD症状。诸如长期氧疗、内皮靶向治疗和药物治疗等干预措施在改善COPD患者寿命以及减缓肺动脉高压进展方面显示出了有前景的结果。在本章中,我们旨在讨论COPD中肺血管重塑的促成因素,重点是ROS,以及针对COPD相关血管重塑的潜在氧化还原治疗方法。

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