ReviewBiomedicines2025
The Role of Ubiquitination and Deubiquitination in the Pathogenesis of Acute Kidney Injury: Progress in Research.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- Ubiquitylation and Deubiquitylation in Health and Diseases.Biomedicines · 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
4 authors.
Funding
Abstract
Acute kidney injury (AKI) remains a critical clinical challenge due to its complex pathophysiology and lack of targeted therapies. We hypothesize that the ubiquitin-proteasome system (UPS) and ubiquitin-like modifiers (UBLs) are not merely isolated players but constitute an intricate and coordinated regulatory network whose dysregulation is a central driving force in AKI progression. This review synthesizes the pivotal roles of the ubiquitin-proteasome system and ubiquitin-like modifiers in driving AKI progression, emphasizing their regulation of inflammatory responses, cell death pathways (apoptosis, pyroptosis, ferroptosis), mitochondrial dysfunction, and aberrant repair. We detail enzymatic cascades involving E1-E2-E3 ligases, deubiquitinating enzymes, and ubiquitin-like modifiers (SUMOylation, neddylation, ISGylation, UFMylation), highlighting their integration into a coordinated network modulating NF-κB/NLRP3 signaling, mitophagy, and growth factor pathways, thereby providing novel strategies for targeted therapy.
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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.