ArticleAutophagy2025
Inflammatory signaling attenuates spliceosome function and cognitive ability.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- A biosafe mouse model for SARS-CoV-2 infection that more realistically simulates COVID-19 symptoms.Signal transduction and targeted therapy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive impairment is a complex condition with diverse causes, but the underlying mechanisms remain elusive. In this study, to explore whether and how inflammation affects cognitive impairment, we adopted two inflammation mouse models, coronavirus disease 2019 (COVID-19) inflammation and acute kidney injury (AKI)-induced inflammation. We observed that the inflammatory response caused accumulation of the oligomer marker derived from the short form of cleaved APP in the brain and cognitive impairment, which was associated with inflammation-induced activation of FGF2 in the mice. Notably, upon FGF2 activation, the HNRNPA1 was partially translocated from the nucleus to the cytoplasm and was degraded by macroautophagy/autophagy. Concurrently, a decrease in the nuclear HNRNPA1 levels impaired autophagy ability through downregulating ATG16L1α isoform via skipped exons in the brain of inflammation mice, thus attenuating autophagic clearance of the oligomers in the brain. The accumulation of the oligomers in the hippocampus region and cognitive impairment were also detected in FGF2-treated mice, owing to autophagy downregulation. Moreover, inhibiting FGF2 signaling via erdafitinib, an inhibitor of FGFR (fibroblast growth factor receptor) protein, partially restored autophagy and cognitive ability. Notably, autophagy ability was upregulated and the corresponding cognitive impairment were rescued in the
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.