ArticleActa pharmacologica Sinica2026
Trim47 protects against hypoxic-ischaemic brain injury in neonatal rats by reducing brain microvascular endothelial inflammation and BBB disruption by interacting with ZO1.
Article in Acta pharmacologica Sinica, 2026. 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
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxic-ischaemic (HI) brain damage is the main contributor to neonatal brain damage and neurodevelopmental impairments. The E3 ubiquitin ligase tripartite motif 47 (Trim47) plays pivotal roles in regulating inflammation, autophagy, and apoptosis in the pathological processes of various diseases. However, the role of Trim47 in neonatal HI brain injury remains unknown. In vivo and in vitro models of neonatal rat brain HI and OGD/R-treated brain microvascular endothelial cells were established to investigate the roles of Trim47 and its underlying regulatory mechanism in neonatal brain injury. We found that Trim47 was highly expressed in brain microvascular endothelial cells, astrocytes and microglia and was downregulated in brain microvascular endothelial cells after neonatal HI injury in vivo and in vitro. Trim47 overexpression attenuated neonatal brain injury and blood-brain barrier (BBB) disruption following HI injury. It also improved long-term neurological outcomes and brain atrophy after HI injury. Trim47 overexpression increased the expression of the tight junction proteins ZO1 and occludin and suppressed MMP9 and AQP4 expression in brain microvascular endothelial cells after OGD/R. It also improved BBB function through ubiquitin conjugation to ZO1 and attenuated brain microvascular endothelial inflammation by suppressing NF-κB activation after OGD/R. However, Trim47 knockdown had the opposite effects. Thus, the present study demonstrates that the neuroprotective role of Trim47 in brain damage is achieved by preserving BBB function through interaction with ZO1 and by reducing brain microvascular endothelial inflammation through the suppression of NF-κB activation after neonatal HI injury.
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.