期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 17, 页码 -出版社
MDPI
DOI: 10.3390/ijms21176421
关键词
hypobaric hypoxia; cardiac hypertrophy; oxidative stress; kinases; inflammation; heart failure
资金
- FIC GORE-TARAPACA [BIP-30477541-0]
High altitude (hypobaric hypoxia) triggers several mechanisms to compensate for the decrease in oxygen bioavailability. One of them is pulmonary artery vasoconstriction and its subsequent pulmonary arterial remodeling. These changes can lead to pulmonary hypertension and the development of right ventricular hypertrophy (RVH), right heart failure (RHF) and, ultimately to death. The aim of this review is to describe the most recent molecular pathways involved in the above conditions under this type of hypobaric hypoxia, including oxidative stress, inflammation, protein kinases activation and fibrosis, and the current therapeutic approaches for these conditions. This review also includes the current knowledge of long-term chronic intermittent hypobaric hypoxia. Furthermore, this review highlights the signaling pathways related to oxidative stress (Nox-derived O(2)(.-)and H2O2), protein kinase (ERK5, p38 alpha and PKC alpha) activation, inflammatory molecules (IL-1 beta, IL-6, TNF-alpha and NF-kB) and hypoxia condition (HIF-1 alpha). On the other hand, recent therapeutic approaches have focused on abolishing hypoxia-induced RVH and RHF via attenuation of oxidative stress and inflammatory (IL-1 beta, MCP-1, SDF-1 and CXCR-4) pathways through phytotherapy and pharmacological trials. Nevertheless, further studies are necessary.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据