Caveolin-1: a critical regulator of lung injury

被引:99
|
作者
Jin, Yang [1 ]
Lee, Seon-Jin [1 ]
Minshall, Richard D. [2 ,3 ]
Choi, Augustine M. K. [1 ]
机构
[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care Med,Dept Med, Boston, MA 02115 USA
[2] Univ Illinois, Ctr Lung & Vasc Biol, Dept Anesthesiol, Chicago, IL USA
[3] Univ Illinois, Ctr Lung & Vasc Biol, Dept Pharmacol, Chicago, IL USA
关键词
apoptosis; inflammation; caveolae; NITRIC-OXIDE SYNTHASE; SIGNAL-TRANSDUCTION PATHWAYS; PULMONARY EPITHELIAL-CELLS; RECEPTOR TYROSINE KINASE; ANTIGEN-PRESENTING CELLS; ENDOTHELIAL-CELLS; IN-VIVO; HEME OXYGENASE-1; LIPID RAFTS; SCAFFOLDING DOMAIN;
D O I
10.1152/ajplung.00170.2010
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Jin Y, Lee SJ, Minshall RD, Choi AM. Caveolin-1: a critical regulator of lung injury. Am J Physiol Lung Cell Mol Physiol 300: L151-L160, 2011. First published November 19, 2010; doi:10.1152/ajplung.00170.2010.-Caveolin-1 (cav-1), a 22-kDa transmembrane scaffolding protein, is the principal structural component of caveolae. Cav-1 regulates critical cell functions including proliferation, apoptosis, cell differentiation, and transcytosis via diverse signaling pathways. Abundant in almost every cell type in the lung, including type I epithelial cells, endothelial cells, smooth muscle cells, fibroblasts, macrophages, and neutrophils, cav-1 plays a crucial role in the pathogenesis of acute lung injury (ALI). ALI and its severe form, acute respiratory distress syndrome (ARDS), are responsible for significant morbidity and mortality in intensive care units, despite improvement in ventilation strategies. The pathogenesis of ARDS is still poorly understood, and therapeutic options remain limited. In this article, we summarize recent data regarding the regulation and function of cav-1 in lung biology and pathology, in particular as it relates to ALI. We further discuss the potential molecular and cellular mechanisms by which cav-1 expression contributes to ALI. Investigating the cellular functions of cav-1 may provide new insights for understanding the pathogenesis of ALI and provide novel targets for therapeutic interventions in the future.
引用
收藏
页码:L151 / L160
页数:10
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