ArticleStroke and vascular neurology2024
APE1 regulates mitochondrial DNA damage repair after experimental subarachnoid haemorrhage in vivo and in vitro.
Article in Stroke and vascular neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Expression of Active Apurinic Apyrimidinic Endodeoxyribonuclease 1 in Human Platelets.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- PDZD8 overexpression alleviates early brain injury via regulating MERCs integrity after experimental subarachnoid hemorrhage.Journal of neuroinflammation · 2026Article
- Spotlight on cGAS-STING: role in disease pathogenesis and therapeutic potential.Molecular biomedicine · 2026Review
- Review
- Iron-driven secondary injury after intracranial hemorrhage: mitochondrial dysfunction and ferroptosis.Frontiers in neuroscience · 2026Review
- Altered Mitochondrial DNA Copy Number and Telomere Length in Patients with Substance Use Disorder: Correlation with Age, Sex, and Chronic Diseases.Biochemical genetics · 2025Article
- Teniposide Triggers DNA Repair Inhibition by Binding and Ubiquitination of Apurinic/Apyrimidinic Endonuclease 1 to Boost Oxidative DNA Damage for Lung Cancer Destruction.ACS pharmacology & translational science · 2025Article
- Unveiling BID: a key biomarker in apoptosis post-intracerebral hemorrhage.Frontiers in neurology · 2025Article
- Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.Chinese neurosurgical journal · 2024Review
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
backgroundSubarachnoid haemorrhage (SAH) can result in a highly unfavourable prognosis. In recent years, the study of SAH has focused on early brain injury (EBI), which is a crucial progress that contributes to adverse prognosis. SAH can lead to various complications, including mitochondrial dysfunction and DNA damage. Apurinic/apyrimidinic endonuclease 1 (APE1) is an essential protein with multifaceted functionality integral to DNA repair and redox signalling. However, the role of APE1 in mitochondrial DNA damage repair after SAH is still unclear.
methodsOur study involved an in vivo endovascular perforation model in rats and an in vitro neuron oxyhaemoglobin intervention. Then, the effects of APE1 on mitochondrial DNA damage repair were analysed by western blot, immunofluorescence, quantitative real-time PCR, mitochondrial bioenergetics measurement and neurobehavioural experiments.
resultsWe found that the level of APE1 decreased while the mitochondria DNA damage and neuronal death increased in a rat model of SAH. Overexpression of APE1 improved short-term and long-term behavioural impairment in rats after SAH. In vitro, after primary neurons exposed to oxyhaemoglobin, APE1 expression significantly decreased along with increased mitochondrial DNA damage, a reduction in the subunit of respiratory chain complex levels and subsequent respiratory chain dysfunction. Overexpression of APE1 relieved energy metabolism disorders in the mitochondrial of neurons and reduced neuronal apoptosis.
conclusionIn conclusion, APE1 is involved in EBI after SAH by affecting mitochondrial apoptosis via the mitochondrial respiratory chain. APE1 may potentially play a vital role in the EBI stage after SAH, making it a critical target for treatment.
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