ReviewTissue barriers2026
Deubiquitinating enzymes at the crossroads of blood-brain barrier integrity and neurodegeneration: mechanistic insights, therapeutic targeting and future directions.
Review in Tissue barriers, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Novel Small-Molecule Analogues of IU1 Ameliorate Amyloid-β Mediated Toxicity in Alzheimer's Disease Cell and Worm Models.International journal of molecular sciences · 2026Article
- Ubiquitin-specific protease 25: a new regulator for cardiovascular and cerebrovascular diseases.Frontiers in cell and developmental biology · 2026Review
- Deubiquitinating enzymes in parkinson's disease: molecular mechanisms and therapeutic potential.Molecular medicine (Cambridge, Mass.) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ubiquitin-proteasome system (UPS) carries immense significance concerning cellular homeostasis that encompasses both ubiquitination and deubiquitination as key facets for maintaining protein stability. The deubiquitinating enzymes (DUBs) have emerged as critical regulators of proteostasis, neuroinflammation and blood-brain barrier (BBB) integrity by controlling the fate of crucial proteins associated with barrier architectures in CNS and neurodegenerative disorders (NDs) alike. However, a concrete understanding of their specific neurodevelopmental and neuroprotective functions is yet to be discerned. This article discusses the multifaceted roles of DUBs in the maintenance of BBB integrity, neuroprotection and various NDs and also underscores the therapeutic prospects targeting the same. While DUBs like USP7, USP9X, USP27X, UCHL1, etc. participate in neural stem cell maintenance and neurogenesis, including BBB function, USP13, USP14, USP25, BRCC3 and CYLD, among others, are associated with BBB dysfunction and NDs. The mechanistic underpinning concerning their hitherto unexplored mode of action, DUB-substrate interactions and specificity would facilitate developing the therapeutic agonists and small-molecule inhibitors to prevent or reverse neuroinflammation, BBB impairment and developmental disorders. Recent innovations concerning DUB-targeting chimaeras (DUBTACs) and proteolysis-targeting chimaeras (PROTACs) can be explored further for their plausible administration via nanoparticle-based delivery approaches to alleviate the progressive neurodegeneration.
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.