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窖蛋白-1:肺损伤的关键调节因子。

Caveolin-1: a critical regulator of lung injury.

机构信息

Division of Pulmonary and Critical Care Medicine, Dept. of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Am J Physiol Lung Cell Mol Physiol. 2011 Feb;300(2):L151-60. doi: 10.1152/ajplung.00170.2010. Epub 2010 Nov 19.

Abstract

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.

摘要

窖蛋白-1(cav-1),一种 22kDa 的跨膜支架蛋白,是小窝的主要结构成分。cav-1 通过多种信号通路调节包括增殖、凋亡、细胞分化和转胞吞作用在内的关键细胞功能。窖蛋白-1 丰富存在于肺的几乎所有细胞类型中,包括 I 型上皮细胞、内皮细胞、平滑肌细胞、成纤维细胞、巨噬细胞和中性粒细胞,在急性肺损伤(ALI)的发病机制中发挥着关键作用。尽管通气策略有所改进,但急性肺损伤(ALI)及其严重形式急性呼吸窘迫综合征(ARDS)仍在重症监护病房导致了显著的发病率和死亡率。ARDS 的发病机制仍不清楚,治疗选择仍然有限。本文总结了有关 cav-1 在肺生物学和病理学中的调节和功能的最新数据,特别是与 ALI 相关的内容。我们进一步讨论了 cav-1 表达导致 ALI 的潜在分子和细胞机制。研究 cav-1 的细胞功能可能为理解 ALI 的发病机制提供新的见解,并为未来的治疗干预提供新的靶点。

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