ArticleInternational journal of molecular sciences2015
Mitochondrial Optic Atrophy (OPA) 1 Processing Is Altered in Response to Neonatal Hypoxic-Ischemic Brain Injury.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 60 citations in OpenAlex.
- Zinc dyshomeostasis, mitochondrial dysfunction, and their pathological cycle in ischemic stroke pathophysiology: Mechanisms and potential therapeutic targets.Redox biology · 2026Review
- The Role of Mitochondria in Obstructive Sleep Apnea: Implications for the Upper Airway Muscles.International journal of molecular sciences · 2025Review
- Novel purine derivatives mitigate hypoxia ischemia related brain injury through agrin, zyxin and synaptotagmin proteins.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Repeated Low-Level Inflammatory Challenge Leads to Alterations in the TNF-CXCL10 Signalling Pathway in Mouse Cerebral Endothelial Cells In Vitro.Journal of neurochemistry · 2025Article
- Mitochondrial membrane potential and oxidative stress interact to regulate Oma1-dependent processing of Opa1 and mitochondrial dynamics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Role of mitochondria in neonatal hypoxic-ischemic encephalopathy.Histology and histopathology · 2024Review
- Leflunomide Treatment Does Not Protect Neural Cells following Oxygen-Glucose Deprivation (OGD) In Vitro.Cells · 2024Article
- Cell death in development, maintenance, and diseases of the nervous system.Seminars in immunopathology · 2022Review
- Mitochondrial Proteins Unveil the Mechanism by Which Physical Exercise Ameliorates Memory, Learning and Motor Activity in Hypoxic Ischemic Encephalopathy Rat Model.International journal of molecular sciences · 2022Article
- Article
- Mitochondrial dynamics in the neonatal brain - a potential target following injury?Bioscience reports · 2022Review
- EPO activates PI3K-IKKα-CDK1 signaling pathway to promote the proliferation of Glial Cells under hypoxia environment.Genetics and molecular biology · 2022Article
- Revealing the Impact of Mitochondrial Fitness During Early Neural Development Using Human Brain Organoids.Frontiers in molecular neuroscience · 2022Review
- Analysis of Mitochondrial Dysfunction by Microplate Reader in hiPSC-Derived Neuronal Cell Models of Neurodegenerative Disorders.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Mitochondrial Dynamics, Mitophagy, and Mitochondria-Endoplasmic Reticulum Contact Sites Crosstalk Under Hypoxia.Frontiers in cell and developmental biology · 2022Review
- Review
- Mitochondrial Quality Control in Cerebral Ischemia-Reperfusion Injury.Molecular neurobiology · 2021Review
- HIGD‑1B inhibits hypoxia‑induced mitochondrial fragmentation by regulating OPA1 cleavage in cardiomyocytes.Molecular medicine reports · 2021Article
- Potential biomarkers and targets of mitochondrial dynamics.Clinical and translational medicine · 2021Review
- Sirtuin 5 depletion impairs mitochondrial function in human proximal tubular epithelial cells.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Perturbation of mitochondrial function and subsequent induction of cell death pathways are key hallmarks in neonatal hypoxic-ischemic (HI) injury, both in animal models and in term infants. Mitoprotective therapies therefore offer a new avenue for intervention for the babies who suffer life-long disabilities as a result of birth asphyxia. Here we show that after oxygen-glucose deprivation in primary neurons or in a mouse model of HI, mitochondrial protein homeostasis is altered, manifesting as a change in mitochondrial morphology and functional impairment. Furthermore we find that the mitochondrial fusion and cristae regulatory protein, OPA1, is aberrantly cleaved to shorter forms. OPA1 cleavage is normally regulated by a balanced action of the proteases Yme1L and Oma1. However, in primary neurons or after HI in vivo, protein expression of YmelL is also reduced, whereas no change is observed in Oma1 expression. Our data strongly suggest that alterations in mitochondria-shaping proteins are an early event in the pathogenesis of neonatal HI injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.