ArticleCell death & disease2020
Overexpression of apoptosis inducing factor aggravates hypoxic-ischemic brain injury in neonatal mice.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Parthenolide Exerts Protection against Hypoxic-Ischemic Brain Damage in Neonatal Rats by Inhibiting Perk-Mediated Endoplasmic Reticulum Stress.Molecular neurobiology · 2025Article
- Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Role of mitochondria in neonatal hypoxic-ischemic encephalopathy.Histology and histopathology · 2024Review
- The lncRNA lnc_AABR07044470.1 promotes the mitochondrial-damaged inflammatory response to neuronal injury via miR-214-3p/PERM1 axis in acute ischemic stroke.Molecular biology reports · 2024Article
- Isobavachalcone exhibits antifungal and antibiofilm effects againstFrontiers in cellular and infection microbiology · 2024Article
- Causal relationship between mitochondrial-associated proteins and cerebral aneurysms: a Mendelian randomization study.Frontiers in neurology · 2024Article
- Apoptosis-inducing factor: a mitochondrial protein associated with metabolic diseases-a narrative review.Cardiovascular diagnosis and therapy · 2023Review
- Potential role of PANoptosis in neuronal cell death: commentary on "PANoptosis-like cell death in ischemia/reperfusion injury of retinal neurons".Neural regeneration research · 2023Article
- AIF Overexpression Aggravates Oxidative Stress in Neonatal Male Mice After Hypoxia-Ischemia Injury.Molecular neurobiology · 2022Article
- The Alpha 7 Nicotinic Acetylcholine Receptor Does Not Affect Neonatal Brain Injury.Biomedicines · 2022Article
- 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
- Autophagy Inhibition Reduces Irradiation-Induced Subcortical White Matter Injury Not by Reducing Inflammation, but by Increasing Mitochondrial Fusion and Inhibiting Mitochondrial Fission.Molecular neurobiology · 2022Article
- Ubiquitinated AIF is a major mediator of hypoxia-induced mitochondrial dysfunction and pulmonary artery smooth muscle cell proliferation.Cell & bioscience · 2022Article
- Article
- [Research advances in the role of ferroptosis in neonatal hypoxic-ischemic brain damage].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021Review
- The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status.Journal of neuroinflammation · 2021Review
- Role of apoptosis-inducing factor in perinatal hypoxic-ischemic brain injury.Neural regeneration research · 2021Review
- 6-Gingerol Alleviates Neonatal Hypoxic-Ischemic Cerebral and White Matter Injury and Contributes to Functional Recovery.Frontiers in pharmacology · 2021Article
- Effects of prenatal photobiomodulation treatment on neonatal hypoxic ischemia in rat offspring.Theranostics · 2021Article
Corrections and comments
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Authors and funding
18 authors.
Funding
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Abstract
Apoptosis inducing factor (AIF) has been shown to be a major contributor to neuron loss in the immature brain after hypoxia-ischemia (HI). Indeed, mice bearing a hypomorphic mutation causing reduced AIF expression are protected against neonatal HI. To further investigate the possible molecular mechanisms of this neuroprotection, we generated an AIF knock-in mouse by introduction of a latent transgene coding for flagged AIF protein into the Rosa26 locus, followed by its conditional activation by a ubiquitously expressed Cre recombinase. Such AIF transgenic mice overexpress the pro-apoptotic splice variant of AIF (AIF1) at both the mRNA (5.9 times higher) and protein level (2.4 times higher), but not the brain-specific AIF splice-isoform (AIF2). Excessive AIF did not have any apparent effects on the phenotype or physiological functions of the mice. However, brain injury (both gray and white matter) after neonatal HI was exacerbated in mice overexpressing AIF, coupled to enhanced translocation of mitochondrial AIF to the nucleus as well as enhanced caspase-3 activation in some brain regions, as indicated by immunohistochemistry. Altogether, these findings corroborate earlier studies demonstrating that AIF plays a causal role in neonatal HI brain injury.
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