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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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2021-03, Vol.10 (3), p.569
Main Authors: S Ten, Vadim, Stepanova, Anna A, Ratner, Veniamin, Neginskaya, Maria, Niatsetskaya, Zoya, Sosunov, Sergey, Starkov, Anatoly
Format: Article
Language:English
Subjects:
Adenosine triphosphate
Alveoli
Bioenergetics
brain
Brain injury
Disease
Dysplasia
Encephalopathy
Energy
Hypoxia
Ischemia
Lungs
Membrane permeability
Metabolism
Mitochondria
Mitochondrial permeability transition pore
Myelination
Neonates
Oxidative stress
Phosphorylation
Premature birth
prematurity
proton leak
Reperfusion
Respiration
Review
Reviews
Substantia alba
Traumatic brain injury
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Summary: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.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells10030569