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早产儿氧化应激与呼吸系统疾病

Oxidative Stress and Respiratory Diseases in Preterm Newborns.

机构信息

Neonatal and Pediatric Intensive Care Unit, Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi", University of Messina, 98125 Messina, Italy.

Neonatology Unity, Department of Medicine and Surgery, University of Parma, 43126 Parma, Italy.

出版信息

Int J Mol Sci. 2021 Nov 19;22(22):12504. doi: 10.3390/ijms222212504.

DOI:10.3390/ijms222212504
PMID:34830385
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8625766/
Abstract

Premature infants are exposed to increased generation of reactive oxygen species, and on the other hand, they have a deficient antioxidant defense system. Oxidative insult is a salient part of lung injury that begins as acute inflammatory injury in respiratory distress disease and then evolves into chronic and structural scarring leading to bronchopulmonary dysplasia. Oxidative stress is also involved in the pathogenesis of pulmonary hypertension in newborns through the modulation of the vascular tone and the response to pulmonary vasodilators, with consequent decrease in the density of the pulmonary vessels and thickening of the pulmonary arteriolar walls. Oxidative stress has been recognized as both a trigger and an endpoint for several events, including inflammation, hypoxia, hyperoxia, drugs, transfusions, and mechanical ventilation, with impairment of pulmonary function and prolonged lung damage. Redoxomics is the most fascinating new measure to address lung damage due to oxidative stress. The new challenge is to use omics data to discover a set of biomarkers useful in diagnosis, prognosis, and formulating optimal and individualized neonatal care. The aim of this review was to examine the most recent evidence on the relationship between oxidative stress and lung diseases in preterm newborns. What is currently known regarding oxidative stress-related lung injury pathogenesis and the available preventive and therapeutic strategies are also discussed.

摘要

早产儿会接触到更多的活性氧,而另一方面,他们的抗氧化防御系统不足。氧化损伤是肺部损伤的一个显著特征,它始于呼吸窘迫病的急性炎症损伤,然后发展为慢性和结构性瘢痕,导致支气管肺发育不良。氧化应激也通过调节血管张力和对肺血管扩张剂的反应参与新生儿肺动脉高压的发病机制,从而导致肺血管密度降低和肺小动脉壁增厚。氧化应激已被认为是包括炎症、缺氧、高氧、药物、输血和机械通气在内的多种事件的触发因素和终点,可损害肺功能并导致长期肺损伤。氧化还原组学是应对氧化应激引起的肺部损伤的最新措施。新的挑战是利用组学数据来发现一组在诊断、预后和制定最佳个体化新生儿护理方面有用的生物标志物。本综述的目的是研究最近关于早产儿氧化应激与肺部疾病之间关系的证据。还讨论了与氧化应激相关的肺损伤发病机制以及现有的预防和治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b93/8625766/7c3fa7b782b3/ijms-22-12504-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b93/8625766/7c3fa7b782b3/ijms-22-12504-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b93/8625766/7c3fa7b782b3/ijms-22-12504-g001.jpg

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