Heat shock protein 70 and the acute respiratory distress syndrome

被引:13
作者
Bromberg, Zohar [1 ]
Deutschman, Clifford S. [1 ]
Weiss, Yoram G. [2 ]
机构
[1] Univ Penn, Sch Med, Dept Anesthesia, Dulles 781A HUP,3400 Spruce St, Philadelphia, PA 19104 USA
[2] Hadassah Hebrew Univ Med Ctr, Dept Anesthesia & Crit Care Med, Jerusalem, Israel
关键词
Sepsis; Lung injury; Acute lung injury; Heat shock response; Stress response; Gene therapy;
D O I
10.1007/s00540-005-0308-2
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
In summary, ARDS is a disorder that involves overwhelming inflammation, alterations in protein expression and function, and cell death by apoptosis and necrosis. Each of these abnormalities can be limited or controlled by an appropriate heat shock response, specifically involving induction of HSP-70. Previous studies have demonstrated failure to increase HSP-70 expression following 2CLP. HSP-70 deficiency contributes to inflammation, altered protein expression, and alveolar cell loss in ARDS. We and others have demonstrated that correcting this deficit may protect alveolar cells, reduce functional and morphologic abnormalities, and improve the outcome in experimental ARDS. Several mechanisms by which HSP-70 may exert its attenuating effects in ARDS have been identified. These findings may have important ramifications with regard to the pathogenesis of ARDS and can help direct further investigation and the development of novel therapeutic approaches. © JSA 2005.
引用
收藏
页码:236 / 242
页数:7
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