Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension.
Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension.
复制标题
肺动脉高压中的线粒体代谢、氧化还原和钙稳态
DOI:
10.3390/biomedicines10020341
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发表时间:
2022-02-01
期刊:
影响因子:
4.7
通讯作者:
Tang H
中科院分区:
文献类型:
--
作者:
Liang S;Yegambaram M;Wang T;Wang J;Black SM;Tang H
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary arterial pressure due to increased pulmonary vascular resistance, secondary to sustained pulmonary vasoconstriction and excessive obliterative pulmonary vascular remodeling. Work over the last decade has led to the identification of a critical role for metabolic reprogramming in the PAH pathogenesis. It is becoming clear that in addition to its role in ATP generation, the mitochondrion is an important organelle that regulates complex and integrative metabolic- and signal transduction pathways. This review focuses on mitochondrial metabolism alterations that occur in deranged pulmonary vessels and the right ventricle, including abnormalities in glycolysis and glucose oxidation, fatty acid oxidation, glutaminolysis, redox homeostasis, as well as iron and calcium metabolism. Further understanding of these mitochondrial metabolic mechanisms could provide viable therapeutic approaches for PAH patients.
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影响因子:
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作者:
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通讯作者:
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DOI:
10.1152/ajplung.00303.2013
发表时间:
2014-10-01
影响因子:
4.9
作者:
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10.1152/ajplung.00002.2012
发表时间:
2012-07-01
影响因子:
4.9
作者:
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通讯作者:
Gupte, Sachin A.
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