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本文引用的文献

1
Autophagy protein microtubule-associated protein 1 light chain-3B (LC3B) activates extrinsic apoptosis during cigarette smoke-induced emphysema.自噬蛋白微管相关蛋白 1 轻链 3B(LC3B)在香烟烟雾诱导的肺气肿中外在凋亡中激活。
Proc Natl Acad Sci U S A. 2010 Nov 2;107(44):18880-5. doi: 10.1073/pnas.1005574107. Epub 2010 Oct 18.
2
Caveolin-1 regulates leucocyte behaviour in fibrotic lung disease.窖蛋白-1 调节肺纤维化疾病中的白细胞行为。
Ann Rheum Dis. 2010 Jun;69(6):1220-6. doi: 10.1136/ard.2009.117580. Epub 2010 Apr 21.
3
MMTV promoter-regulated caveolin-1 overexpression yields defective parenchymal epithelia in multiple exocrine organs of transgenic mice.MMTV 启动子调控的 caveolin-1 过表达导致转基因小鼠多个外分泌腺实质上皮的缺陷。
Exp Mol Pathol. 2010 Aug;89(1):9-19. doi: 10.1016/j.yexmp.2010.03.009. Epub 2010 Apr 22.
4
A novel insight into the mechanism of pulmonary hypertension involving caveolin-1 deficiency and endothelial nitric oxide synthase activation.一种新的见解揭示了涉及 caveolin-1 缺乏和内皮型一氧化氮合酶激活的肺动脉高压的机制。
Trends Cardiovasc Med. 2009 Oct;19(7):238-42. doi: 10.1016/j.tcm.2010.02.003.
5
Caveolin-1 deficiency dampens Toll-like receptor 4 signaling through eNOS activation.窖蛋白-1 缺乏通过内皮型一氧化氮合酶激活来抑制 Toll 样受体 4 信号通路。
Am J Pathol. 2010 May;176(5):2344-51. doi: 10.2353/ajpath.2010.091088. Epub 2010 Mar 19.
6
Bleomycin induces the extrinsic apoptotic pathway in pulmonary endothelial cells.博来霉素诱导肺内皮细胞发生外在凋亡途径。
Am J Physiol Lung Cell Mol Physiol. 2010 May;298(5):L696-703. doi: 10.1152/ajplung.00322.2009. Epub 2010 Feb 12.
7
Exploring the caves: cavins, caveolins and caveolae.探索洞穴:腔室、窖蛋白和小窝。
Trends Cell Biol. 2010 Apr;20(4):177-86. doi: 10.1016/j.tcb.2010.01.005. Epub 2010 Feb 12.
8
Over-expression of caveolin-1 aggravate LPS-induced inflammatory response in AT-1 cells via up-regulation of cPLA2/p38 MAPK.窖蛋白-1 的过表达通过上调 cPLA2/p38MAPK 加重 LPS 诱导的 AT-1 细胞炎症反应。
Inflamm Res. 2010 Jul;59(7):531-41. doi: 10.1007/s00011-010-0157-9. Epub 2010 Jan 23.
9
Caveolae-mediated entry of Salmonella typhimurium into senescent nonphagocytotic host cells.空泡介导鼠伤寒沙门氏菌进入衰老的非吞噬性宿主细胞。
Aging Cell. 2010 Apr;9(2):243-51. doi: 10.1111/j.1474-9726.2010.00554.x. Epub 2010 Jan 20.
10
Caveolin-1 modifies the immunity to Pseudomonas aeruginosa.窖蛋白-1 修饰对铜绿假单胞菌的免疫反应。
J Immunol. 2010 Jan 1;184(1):296-302. doi: 10.4049/jimmunol.0900604. Epub 2009 Nov 30.

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.

DOI:10.1152/ajplung.00170.2010
PMID:21097526
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4380484/
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。