Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries
This review discusses the potential mechanistic role of abnormally elevated mitochondrial proton leak and mitochondrial bioenergetic dysfunction in the pathogenesis of neonatal brain and lung injuries associated with premature birth. Providing supporting evidence, we hypothesized that mitochondrial...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-03-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/10/3/569 |
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| author | Vadim S. Ten Anna A. Stepanova Veniamin Ratner Maria Neginskaya Zoya Niatsetskaya Sergey Sosunov Anatoly Starkov |
| author_facet | Vadim S. Ten Anna A. Stepanova Veniamin Ratner Maria Neginskaya Zoya Niatsetskaya Sergey Sosunov Anatoly Starkov |
| author_sort | Vadim S. Ten |
| collection | DOAJ |
| description | This review discusses the potential mechanistic role of abnormally elevated mitochondrial proton leak and mitochondrial bioenergetic dysfunction in the pathogenesis of neonatal brain and lung injuries associated with premature birth. Providing supporting evidence, we hypothesized that mitochondrial dysfunction contributes to postnatal alveolar developmental arrest in bronchopulmonary dysplasia (BPD) and cerebral myelination failure in diffuse white matter injury (WMI). This review also analyzes data on mitochondrial dysfunction triggered by activation of mitochondrial permeability transition pore(s) (mPTP) during the evolution of perinatal hypoxic-ischemic encephalopathy. While the still cryptic molecular identity of mPTP continues to be a subject for extensive basic science research efforts, the translational significance of mitochondrial proton leak received less scientific attention, especially in diseases of the developing organs. This review is focused on the potential mechanistic relevance of mPTP and mitochondrial dysfunction to neonatal diseases driven by developmental failure of organ maturation or by acute ischemia-reperfusion insult during development. |
| first_indexed | 2024-03-09T05:19:48Z |
| format | Article |
| id | doaj.art-09e69b44062041269d375e0a97da9328 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-09T05:19:48Z |
| publishDate | 2021-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-09e69b44062041269d375e0a97da93282023-12-03T12:41:17ZengMDPI AGCells2073-44092021-03-0110356910.3390/cells10030569Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung InjuriesVadim S. Ten0Anna A. Stepanova1Veniamin Ratner2Maria Neginskaya3Zoya Niatsetskaya4Sergey Sosunov5Anatoly Starkov6Departments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USADepartments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USADepartment of Pediatrics, Icahn Mount Sinai School of Medicine, New York, NY 10029, USADepartment Molecular Pathobiology, New York University School of Dentistry, New York, NY 10010, USADepartments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USADepartments of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USANeuroscience Department, Weil-Cornell School of Medicine, New York, NY 10065, USAThis review discusses the potential mechanistic role of abnormally elevated mitochondrial proton leak and mitochondrial bioenergetic dysfunction in the pathogenesis of neonatal brain and lung injuries associated with premature birth. Providing supporting evidence, we hypothesized that mitochondrial dysfunction contributes to postnatal alveolar developmental arrest in bronchopulmonary dysplasia (BPD) and cerebral myelination failure in diffuse white matter injury (WMI). This review also analyzes data on mitochondrial dysfunction triggered by activation of mitochondrial permeability transition pore(s) (mPTP) during the evolution of perinatal hypoxic-ischemic encephalopathy. While the still cryptic molecular identity of mPTP continues to be a subject for extensive basic science research efforts, the translational significance of mitochondrial proton leak received less scientific attention, especially in diseases of the developing organs. This review is focused on the potential mechanistic relevance of mPTP and mitochondrial dysfunction to neonatal diseases driven by developmental failure of organ maturation or by acute ischemia-reperfusion insult during development.https://www.mdpi.com/2073-4409/10/3/569prematuritymitochondriaproton leaklungsbrain |
| spellingShingle | Vadim S. Ten Anna A. Stepanova Veniamin Ratner Maria Neginskaya Zoya Niatsetskaya Sergey Sosunov Anatoly Starkov Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries Cells prematurity mitochondria proton leak lungs brain |
| title | Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries |
| title_full | Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries |
| title_fullStr | Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries |
| title_full_unstemmed | Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries |
| title_short | Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries |
| title_sort | mitochondrial dysfunction and permeability transition in neonatal brain and lung injuries |
| topic | prematurity mitochondria proton leak lungs brain |
| url | https://www.mdpi.com/2073-4409/10/3/569 |
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