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肺血管中氧感受和离子通道的发育调控。

Developmental regulation of oxygen sensing and ion channels in the pulmonary vasculature.

机构信息

Divisions of Pediatric Pulmonary, Allergy, and Critical Care Medicine, Stanford University Medical School Medicine, 770 Welch Road, Suite 350, Stanford, CA, 94305, USA.

出版信息

Adv Exp Med Biol. 2010;661:201-20. doi: 10.1007/978-1-60761-500-2_13.

Abstract

The increase in oxygen tension occurring at birth causes sustained and progressive pulmonary vasodilation. The oxygen-induced perinatal pulmonary vasodilation depends on the production of nitric oxide (NO) from the pulmonary endothelium and activation of various K(+) channels in pulmonary artery smooth muscle cells. This chapter reviews a) the oxygen-sensing mechanism that stimulates endothelial NO production; b) how K(+) channels sense changes in oxygen tension; c) whether hypoxia-inducible factor-1alpha (HIF-1alpha), a well defined hypoxia-sensitive transcription factor in adult, contributes to the regulation of NO production and K(+) channel activation; and d) whether and how dysfunctional K(+) channels contribute to the development of pulmonary hypertension in the newborns.

摘要

出生时氧张力的增加导致持续和渐进的肺血管舒张。氧诱导的围产期肺血管舒张依赖于肺内皮细胞产生的一氧化氮(NO)和肺动脉平滑肌细胞中各种 K(+)通道的激活。本章综述了:a)刺激内皮细胞产生 NO 的氧感应机制;b)K(+)通道如何感知氧张力的变化;c)在成人中作为明确的缺氧敏感转录因子的缺氧诱导因子-1α(HIF-1α)是否有助于 NO 产生和 K(+)通道激活的调节;d)K(+)通道功能障碍是否以及如何导致新生儿肺动脉高压的发展。

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