ArticleCNS neuroscience & therapeutics2025
Phosphorylation of cAMP-Activated Exchange Protein-1 Participates in Neuroprotection and Ferroptosis Regulation Following Intracerebral Hemorrhage in Rats.
Article in CNS neuroscience & therapeutics, 2025. 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
7 authors.
Funding
Abstract
backgroundIntracerebral hemorrhage (ICH) is a severe condition characterized by elevated mortality and disability rates. The cAMP-activated exchange protein-1 (EPAC-1) is implicated in various cytoprotective mechanisms; however, its specific role in ICH remains unclear.
methodsA rat model of ICH was established by injecting autologous blood, while the in vitro primary neuronal model was stimulated using oxyhemoglobin (OxyHb). The construction of EPAC-1 overexpression wild-type (WT) and phosphorylated mutant plasmids (S108A or S108E), as well as lentiviruses, was performed for in vitro and in vivo studies.
resultsThe cAMP signaling pathway was found to be significantly enriched following ICH by high-throughput sequencing analysis. Our findings showed that while EPAC-1 protein levels remained relatively unchanged after ICH, RabGEF activity was conspicuously upregulated. This was accompanied by a marked decrease in EPAC-1 phosphorylation levels. Mutations that activate EPAC-1 phosphorylation led to significant improvements in neuronal survival and behavioral outcomes after ICH. Bioinformatics analysis revealed that ferroptosis was significantly enriched after ICH and showed a positive correlation with EPAC-1 serine phosphorylation. EPAC-1 phosphorylation activating mutations inhibit neuronal ferroptosis, whereas inactivating mutations exacerbate it.
conclusionThe phosphorylation of EPAC-1 is essential for maintaining neuronal survival, which may be related to ferroptosis inhibition after ICH.
Indexed as
Identifiers
What Socratic 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 Socratic graph.