ArticleiScience2025
Inhibiting ANP32E protects against acute kidney injury by regulating autophagy via the AMPK pathway.
Article in iScience, 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
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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.
- Autophagy-senescence interplay in kidney disease: mechanistic insights and therapeutic potential.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia-reperfusion (I/R) injury is a secondary injury that frequently occurs during acute kidney injury (AKI) treatment. Acidic nuclear phosphoprotein 32 family member E (ANP32E) disorders are associated with several pathological conditions linked to renal dysfunction. However, the role and mechanism of ANP32E in AKI remain unclear. An AKI mouse model was established by I/R. Additionally, we used microarray technology and
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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.