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高海拔地区的血管稳态:基因变异和转录因子的作用

Vascular homeostasis at high-altitude: role of genetic variants and transcription factors.

作者信息

Chanana Neha, Palmo Tsering, Newman John H, Pasha M A Qadar

机构信息

Genomics and Molecular Medicine, CSIR-Institute of Genomics and Integrative Biology, Delhi, India.

Pulmonary Circulation Center, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.

出版信息

Pulm Circ. 2020 Nov 19;10(4):2045894020913475. doi: 10.1177/2045894020913475. eCollection 2020 Oct-Dec.

DOI:10.1177/2045894020913475
PMID:33282179
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7682230/
Abstract

High-altitude pulmonary edema occurs most frequently in non-acclimatized low landers on exposure to altitude ≥2500 m. High-altitude pulmonary edema is a complex condition that involves perturbation of signaling pathways in vasoconstrictors, vasodilators, anti-diuretics, and vascular growth factors. Genetic variations are instrumental in regulating these pathways and evidence is accumulating for a role of epigenetic modification in hypoxic responses. This review focuses on the crosstalk between high-altitude pulmonary edema-associated genetic variants and transcription factors, comparing high-altitude adapted and high-altitude pulmonary edema-afflicted subjects. This approach might ultimately yield biomarker information both to understand and to design therapies for high-altitude adaptation.

摘要

高原肺水肿最常发生于未适应高原环境的低海拔居民暴露于海拔≥2500米的高度时。高原肺水肿是一种复杂的病症,涉及血管收缩剂、血管扩张剂、抗利尿剂和血管生长因子信号通路的紊乱。基因变异有助于调节这些通路,并且越来越多的证据表明表观遗传修饰在低氧反应中发挥作用。本综述聚焦于高原肺水肿相关基因变异与转录因子之间的相互作用,比较适应高原环境者和患高原肺水肿者。这种方法最终可能会产生生物标志物信息,以帮助理解和设计高原适应疗法。

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