Mitochondrial Dynamics in Pulmonary Hypertension.

Mitochondrial Dynamics in Pulmonary Hypertension.
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肺动脉高压的线粒体动力学。

DOI:
10.3390/biomedicines12010053
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发表时间:
2023-12-25
期刊:
影响因子:
4.7
通讯作者:
--
中科院分区:
工程技术3区
文献类型:
--
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线粒体是参与肺血管生物学和疾病过程中能量产生、钙稳态、氧化还原信号和其他细胞反应的重要细胞器。线粒体的动态平衡依赖于线粒体融合和分裂(动力学)的平衡。线粒体的动态由一个可行的生物钟来调节。低氧和尼古丁暴露可导致线粒体动力学功能障碍,增加线粒体活性氧生成和钙浓度,并减少ATP的产生。这些线粒体改变导致肺血管氧化应激、炎症反应、收缩功能障碍、病理重塑,最终导致肺动脉高压。因此,在这篇综述文章中,我们主要总结了肺血管线粒体代谢中昼夜节律作用的基础、翻译和临床研究的最新进展。这一知识不仅对全面了解肺动脉高压的发展至关重要,而且极大地有助于创造新的治疗策略来治疗这种毁灭性的疾病和其他相关的肺部疾病。
Mitochondria are essential organelles for energy production, calcium homeostasis, redox signaling, and other cellular responses involved in pulmonary vascular biology and disease processes. Mitochondrial homeostasis depends on a balance in mitochondrial fusion and fission (dynamics). Mitochondrial dynamics are regulated by a viable circadian clock. Hypoxia and nicotine exposure can cause dysfunctions in mitochondrial dynamics, increases in mitochondrial reactive oxygen species generation and calcium concentration, and decreases in ATP production. These mitochondrial changes contribute significantly to pulmonary vascular oxidative stress, inflammatory responses, contractile dysfunction, pathologic remodeling, and eventually pulmonary hypertension. In this review article, therefore, we primarily summarize recent advances in basic, translational, and clinical studies of circadian roles in mitochondrial metabolism in the pulmonary vasculature. This knowledge may not only be crucial to fully understanding the development of pulmonary hypertension, but also greatly help to create new therapeutic strategies for treating this devastating disease and other related pulmonary disorders.
DOI: 10.1089/152702903769192269
发表时间: 2003-09-01
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