ArticleFrontiers in neurology2026
Cuproptosis-related molecular alterations in a neonatal rat model of hypoxic-ischemic brain damage.
Article in Frontiers in neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Copper homeostasis imbalance is closely linked to the progression of various neurological disorders. Cuproptosis, a recently identified form of cell death caused by abnormal intracellular copper accumulation, has an unclear relationship with hypoxic-ischemic brain damage (HIBD). This study aims to characterize cuproptosis-associated molecular changes in the pathological process of HIBD in neonatal rats. Methods: A neonatal rat HIBD model was established using the modified Rice-Vannucci method. Cerebral blood flow was measured with laser Doppler flowmetry, while infarct volume was assessed through 2,3,5-triphenyltetrazolium chloride staining. To evaluate brain tissue damage and mitochondrial ultrastructural changes, histological staining and transmission electron microscopy were utilized. Specific assay kits were used to detect oxidative stress markers and copper ion levels in the brain tissue. Immunofluorescence staining was employed to monitor DLAT expression in neural cells, and Western blotting was conducted to analyze the expression of cuproptosis-related proteins. Results: Compared to the Sham group, the HIBD group exhibited significantly reduced perfusion in the injured cerebral hemisphere, which was associated with liquefactive necrosis and tissue atrophy. Additionally, increased levels of copper ions and ROS, along with decreased levels of GSH and GPX4, indicated that HIBD leads to copper dyshomeostasis and oxidative stress. Staining results showed glial cell activation, neuronal loss, and widespread downregulation of DLAT expression in the HIBD group, suggesting the presence of neuroinflammatory responses and cellular metabolic disturbances. Furthermore, the upregulation of cuproptosis-related proteins FDX1 and HSP70, along with the downregulation of LIAS, ACO2, and Lip-DLAT, and such molecular changes correlate with impaired lipoylation metabolism and iron-sulfur cluster biosynthesis, aligning with molecular signatures of cuproptosis. Conclusion: This study identifies multiple cuproptosis-related molecular alterations coinciding with neuronal injury after HIBD in neonatal rats; these changes are accompanied by impaired lipoylation modification and disrupted redox homeostasis.
Indexed as
Identifiers
What OpenQuestion holds
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.