ArticleCells2022
Induction of Mitochondrial Fragmentation and Mitophagy after Neonatal Hypoxia-Ischemia.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Hypoxia Triggers BNIP3/BNIP3L-Associated Mitophagy in HT22 Immortalized Hippocampal Neurons: A Temporal Descriptive Study.Biology · 2026Article
- Article
- Heme oxygenase-1 induction by hemin: a novel approach to enhance mitochondrial turnover and mitigate diet-induced liver damage.Journal of physiology and biochemistry · 2026Article
- Mitochondrial dysfunction in neonatal brain injury: from molecular mechanisms to therapeutic interventions.Journal of translational medicine · 2026Review
- Exosomes in organ transplantation: roles in immunomodulation, ferroptosis and mitophagy.Frontiers in immunology · 2026Review
- Excessive mitochondrial fission and associated extracellular mitochondria mediate cardiac dysfunction in obesity cardiomyopathy.Life sciences · 2025Article
- The role of cardiolipin in mitochondrial dynamics and quality control in neuronal ischemia/reperfusion injury.Cell death & disease · 2025Review
- Mitochondrial dynamics and quality control regulate proteostasis in neuronal ischemia-reperfusion.Autophagy · 2025Article
- Agent-based modeling of neuronal mitochondrial dynamics using intrinsic variables of individual mitochondria.iScience · 2025Article
- PHLDA1 contributes to hypoxic ischemic brain injury in neonatal rats via inhibiting FUNDC1-mediated mitophagy.Acta pharmacologica Sinica · 2024Article
- Metabolic and Microbial Dysregulation in Preterm Infants with Neonatal Respiratory Distress Syndrome: An Early Developmental Perspective.Journal of proteome research · 2024Article
- Role of mitochondria in neonatal hypoxic-ischemic encephalopathy.Histology and histopathology · 2024Review
- Regulated cell death in hypoxic-ischaemic encephalopathy: recent development and mechanistic overview.Cell death discovery · 2024Review
- Leflunomide Treatment Does Not Protect Neural Cells following Oxygen-Glucose Deprivation (OGD) In Vitro.Cells · 2024Article
- Effects of honokiol protects against chronic kidney disease via BNIP3/NIX and FUNDC1-mediated mitophagy and AMPK pathways.Molecular biology reports · 2023Article
- The Oxygen and Glucose Deprivation of Immature Cells of the Nervous System Exerts Distinct Effects on Mitochondria, Mitophagy, and Autophagy, Depending on the Cells' Differentiation Stage.Brain sciences · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Hypoxia-ischemia (HI) leads to immature brain injury mediated by mitochondrial stress. If damaged mitochondria cannot be repaired, mitochondrial permeabilization ensues, leading to cell death. Non-optimal turnover of mitochondria is critical as it affects short and long term structural and functional recovery and brain development. Therefore, disposal of deficient mitochondria via mitophagy and their replacement through biogenesis is needed. We utilized mt-Keima reporter mice to quantify mitochondrial morphology (fission, fusion) and mitophagy and their mechanisms in primary neurons after Oxygen Glucose Deprivation (OGD) and in brain sections after neonatal HI. Molecular mechanisms of PARK2-dependent and -independent pathways of mitophagy were investigated in vivo by PCR and Western blotting. Mitochondrial morphology and mitophagy were investigated using live cell microscopy. In primary neurons, we found a primary fission wave immediately after OGD with a significant increase in mitophagy followed by a secondary phase of fission at 24 h following recovery. Following HI, mitophagy was upregulated immediately after HI followed by a second wave at 7 days. Western blotting suggests that both PINK1/Parkin-dependent and -independent mechanisms, including NIX and FUNDC1, were upregulated immediately after HI, whereas a PINK1/Parkin mechanism predominated 7 days after HI. We hypothesize that excessive mitophagy in the early phase is a pathologic response which may contribute to secondary energy depletion, whereas secondary mitophagy may be involved in post-HI regeneration and repair.
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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 Socratic graph.