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病毒感染和衰老作为肺纤维化发展的协同因素。

Viral infection and aging as cofactors for the development of pulmonary fibrosis.

机构信息

Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI 48109-2200, USA.

出版信息

Expert Rev Respir Med. 2010 Dec;4(6):759-71. doi: 10.1586/ers.10.73.

Abstract

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown origin and progression that primarily affects older adults. Accumulating clinical and experimental evidence suggests that viral infections may play a role, either as agents that predispose the lung to fibrosis or exacerbate existing fibrosis. In particular, herpesviruses have been linked with IPF. This article summarizes the evidence for and against viral cofactors in IPF pathogenesis. In addition, we review mechanistic studies in animal models that highlight the fibrotic potential of viral infection, and explore the different mechanisms that might be responsible. We also review early evidence to suggest that the aged lung may be particularly susceptible to viral-induced fibrosis and make recommendations for future research directions.

摘要

特发性肺纤维化(IPF)是一种病因不明且进展缓慢的疾病,主要影响老年人。越来越多的临床和实验证据表明,病毒感染可能起作用,要么作为使肺部易于发生纤维化的因素,要么作为加重现有纤维化的因素。特别是,疱疹病毒与 IPF 有关。本文总结了病毒在 IPF 发病机制中的辅助作用的证据。此外,我们还回顾了动物模型中的机制研究,这些研究强调了病毒感染的纤维化潜力,并探讨了可能起作用的不同机制。我们还回顾了早期的证据,表明衰老的肺部可能特别容易受到病毒引起的纤维化,并为未来的研究方向提出建议。

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