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呼吸机相关性肺损伤:基因激活的作用。

Ventilator-induced lung injury: the role of gene activation.

机构信息

University Children's Medical Institute, National University Health System, Singapore, Singapore.

出版信息

Curr Opin Crit Care. 2012 Feb;18(1):16-22. doi: 10.1097/MCC.0b013e32834e7d00.

DOI:10.1097/MCC.0b013e32834e7d00
PMID:22157252
Abstract

PURPOSE OF REVIEW

Ventilator-induced lung injury (VILI) is a ubiquitous iatrogenic clinical problem in critical care. Aside from avoiding large tidal volumes, little progress has been made in identifying effective clinical strategies to minimize this injury. With recent rapid development in bioinformatics and high-throughput molecular technology, the genetic basis of lung injury has been intensively investigated. This review will describe recent insights and potential therapies developed in the field.

RECENT FINDINGS

Much progress has been made in delineating the possible genes and gene products involved in VILI through various mechanisms such as early induced genes, capillary leak, apoptosis, fibrin deposition, inflammatory cytokines, oxidative stress, disrupted angiogenesis, and neutrophil infiltration. Some studies have translated bench findings to the bedside in an attempt to identify clinically important genetic susceptibility, which could aid in the identification of at-risk individuals who might benefit from careful titration of mechanical ventilation. Genetic insights also provide candidate pharmaceutical approaches that may ameliorate VILI in the future.

SUMMARY

Much relevant information exists for investigators and clinicians interested in VILI. Future research will interlink evolving data to provide a more integrated picture of the molecular mechanisms involved in VILI enabling translation of the most promising candidate therapies.

摘要

目的综述

呼吸机相关性肺损伤(VILI)是重症监护中普遍存在的医源性临床问题。除了避免大潮气量外,在确定有效临床策略以最小化这种损伤方面几乎没有取得进展。随着生物信息学和高通量分子技术的快速发展,肺损伤的遗传基础得到了深入研究。本综述将描述该领域最近的研究进展和潜在治疗方法。

最新发现

通过早期诱导基因、毛细血管渗漏、细胞凋亡、纤维蛋白沉积、炎症细胞因子、氧化应激、血管生成障碍和中性粒细胞浸润等多种机制,在描述可能涉及 VILI 的基因和基因产物方面取得了很大进展。一些研究已经将实验室研究结果转化为临床,试图确定临床上重要的遗传易感性,这有助于识别可能受益于机械通气仔细滴定的高危个体。遗传研究还为未来可能改善 VILI 的药物治疗提供了候选方法。

总结

对于关注 VILI 的研究人员和临床医生来说,有很多相关信息。未来的研究将结合不断发展的数据,提供一个更全面的 VILI 相关分子机制的图片,使最有希望的候选治疗方法能够得到转化。

相似文献

1
Ventilator-induced lung injury: the role of gene activation.呼吸机相关性肺损伤:基因激活的作用。
Curr Opin Crit Care. 2012 Feb;18(1):16-22. doi: 10.1097/MCC.0b013e32834e7d00.
2
A critical role for gelsolin in ventilator-induced lung injury.凝溶胶蛋白在呼吸机诱导的肺损伤中起关键作用。
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The role of cytokines during the pathogenesis of ventilator-associated and ventilator-induced lung injury.细胞因子在呼吸机相关性和呼吸机诱导性肺损伤发病机制中的作用。
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Oxidant stress mediates inflammation and apoptosis in ventilator-induced lung injury.氧化应激介导呼吸机所致肺损伤中的炎症反应和细胞凋亡。
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Ventilator-induced lung injury and sepsis: two sides of the same coin?呼吸机相关性肺损伤与脓毒症:同一枚硬币的两面?
Minerva Anestesiol. 2011 Jun;77(6):647-53.
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Neutrophil elastase inhibitor (sivelestat) attenuates subsequent ventilator-induced lung injury in mice.中性粒细胞弹性蛋白酶抑制剂(西维来司他)可减轻小鼠随后发生的呼吸机诱导性肺损伤。
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Role for nuclear factor-kappaB in augmented lung injury because of interaction between hyperoxia and high stretch ventilation.核因子-κB在高氧与高张通气相互作用所致的肺损伤加重中的作用。
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Inflammatory mechanisms of ventilator-induced lung injury: a time to stop and think?呼吸机相关性肺损伤的炎症机制:是时候停下来思考了吗?
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Captopril decreases plasminogen activator inhibitor-1 in rats with ventilator-induced lung injury.卡托普利可降低呼吸机诱导性肺损伤大鼠的纤溶酶原激活物抑制剂-1水平。
Crit Care Med. 2008 Jun;36(6):1880-5. doi: 10.1097/CCM.0b013e31817c911d.
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Cytokines and biotrauma in ventilator-induced lung injury: a critical review of the literature.呼吸机诱导性肺损伤中的细胞因子与生物创伤:文献综述
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