Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension
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 h...
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MDPI AG
2022-02-01
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| Series: | Biomedicines |
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| Online Access: | https://www.mdpi.com/2227-9059/10/2/341 |
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| author | Shuxin Liang Manivannan Yegambaram Ting Wang Jian Wang Stephen M. Black Haiyang Tang |
| author_facet | Shuxin Liang Manivannan Yegambaram Ting Wang Jian Wang Stephen M. Black Haiyang Tang |
| author_sort | Shuxin Liang |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-09T22:33:19Z |
| format | Article |
| id | doaj.art-de2fd480cdad42438e57664e94af562f |
| institution | Directory Open Access Journal |
| issn | 2227-9059 |
| language | English |
| last_indexed | 2024-03-09T22:33:19Z |
| publishDate | 2022-02-01 |
| publisher | MDPI AG |
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| series | Biomedicines |
| spelling | doaj.art-de2fd480cdad42438e57664e94af562f2023-11-23T18:54:05ZengMDPI AGBiomedicines2227-90592022-02-0110234110.3390/biomedicines10020341Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial HypertensionShuxin Liang0Manivannan Yegambaram1Ting Wang2Jian Wang3Stephen M. Black4Haiyang Tang5State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangdong Key Laboratory of Vascular Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, ChinaCenter for Translational Science, 11350 SW Village Pkwy, Port St. Lucie, FL 34987, USACenter for Translational Science, 11350 SW Village Pkwy, Port St. Lucie, FL 34987, USAState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangdong Key Laboratory of Vascular Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, ChinaCenter for Translational Science, 11350 SW Village Pkwy, Port St. Lucie, FL 34987, USAState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangdong Key Laboratory of Vascular Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, ChinaPulmonary 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.https://www.mdpi.com/2227-9059/10/2/341metabolismmitochondriapulmonary hypertension |
| spellingShingle | Shuxin Liang Manivannan Yegambaram Ting Wang Jian Wang Stephen M. Black Haiyang Tang Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension Biomedicines metabolism mitochondria pulmonary hypertension |
| title | Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension |
| title_full | Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension |
| title_fullStr | Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension |
| title_full_unstemmed | Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension |
| title_short | Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension |
| title_sort | mitochondrial metabolism redox and calcium homeostasis in pulmonary arterial hypertension |
| topic | metabolism mitochondria pulmonary hypertension |
| url | https://www.mdpi.com/2227-9059/10/2/341 |
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