ArticleNeuroscience2016
Sex-dependent mitophagy and neuronal death following rat neonatal hypoxia-ischemia.
Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 71 citations in OpenAlex.
- PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury.Frontiers in physiology · 2026Review
- Pituitary adenylate cyclase-activating polypeptide and mitochondrial homeostasis in neuronal injury: mechanisms and translational prospects.Frontiers in immunology · 2026Review
- Sex-Dependent Regional Vulnerability and Recovery Mechanisms in a Mouse Model of Transient Global Cerebral Ischemia.Neuromolecular medicine · 2025Article
- Cell-Type-Specific Autophagy in Human Leukocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Decellularization of various tissues and organs through chemical methods.Tissue & cell · 2024Review
- PHLDA1 contributes to hypoxic ischemic brain injury in neonatal rats via inhibiting FUNDC1-mediated mitophagy.Acta pharmacologica Sinica · 2024Article
- Role of mitochondria in neonatal hypoxic-ischemic encephalopathy.Histology and histopathology · 2024Review
- Gender-specific prognosis models reveal differences in subarachnoid hemorrhage patients between sexes.CNS neuroscience & therapeutics · 2024Article
- Sex-specific associations of kynurenic acid with neopterin in Alzheimer's disease.Alzheimer's research & therapy · 2024Article
- Increased regional activity of a pro-autophagy pathway in schizophrenia as a contributor to sex differences in the disease pathology.Cell reports. Medicine · 2024Article
- The role of autophagy in Parkinson's disease: a gender difference overview.Frontiers in pharmacology · 2024Review
- Intraneuronal β-amyloid impaired mitochondrial proteostasis through the impact on LONP1.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Protective mechanisms of quercetin in neonatal rat brain injury induced by hypoxic-ischemic brain damage (HIBD).Food science & nutrition · 2023Article
- Basal autophagic flux measured in blood correlates positively with age in adults at increased risk of type 2 diabetes.GeroScience · 2023Observational
- 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
- Sex-biased autophagy as a potential mechanism mediating sex differences in ischemic stroke outcome.Neural regeneration research · 2023Review
- Choline Improves Neonatal Hypoxia-Ischemia Induced Changes in Male but Not Female Rats.International journal of molecular sciences · 2022Article
- Article
- Mitochondrial dynamics in the neonatal brain - a potential target following injury?Bioscience reports · 2022Review
- Oestrogenic Regulation of Mitochondrial Dynamics.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Males are more susceptible than females to long-term cognitive deficits following neonatal hypoxic-ischemic encephalopathy (HIE). Mitochondrial dysfunction is implicated in the pathophysiology of cerebral hypoxia-ischemia (HI), but the influence of sex on mitochondrial quality control (MQC) after HI is unknown. Therefore, we tested the hypothesis that mitophagy is sexually dimorphic and neuroprotective 20-24h following the Rice-Vannucci model of rat neonatal HI at postnatal day 7 (PN7). Mitochondrial and lysosomal morphology and degree of co-localization were determined by immunofluorescence in the cerebral cortex. No difference in mitochondrial abundance was detected in the cortex after HI. However, net mitochondrial fission increased in both hemispheres of female brain, but was most extensive in the ipsilateral hemisphere of male brain following HI. Basal autophagy, assessed by immunoblot for the autophagosome marker LC3BI/II, was greater in males suggesting less intrinsic reserve capacity for autophagy following HI. Autophagosome formation, lysosome size, and TOM20/LAMP2 co-localization were increased in the contralateral hemisphere following HI in female, but not male brain. An accumulation of ubiquitinated mitochondrial protein was observed in male, but not female brain following HI. Moreover, neuronal cell death with NeuN/TUNEL co-staining occurred in both hemispheres of male brain, but only in the ipsilateral hemisphere of female brain after HI. In summary, mitophagy induction and neuronal cell death are sex dependent following HI. The deficit in elimination of damaged/dysfunctional mitochondria in the male brain following HI may contribute to male vulnerability to neuronal death and long-term neurobehavioral deficits following HIE.
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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.