ArticleIn vitro cellular & developmental biology. Animal2026
The miR-335-5p/DKK1/autophagy axis regulates TNF-α-mediated dysfunction of dental pulp stem cells.
Article in In vitro cellular & developmental biology. Animal, 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
8 authors.
Funding
Abstract
Dental pulp stem cells (DPSCs) play a critical role in maintaining dental pulp homeostasis and supporting dentin-pulp complex regeneration, while tumor necrosis factor-α (TNF-α)-mediated inflammation severely impairs their biological functions. This study explored the role of the miR-335-5p/DKK1/autophagy axis in TNF-α-induced DPSCs dysfunction. Human DPSCs were stimulated with 20 ng/mL TNF-α; miR-335-5p overexpression and DKK1 silencing were achieved via transfection. qRT-PCR, Western blot, SA-β-gal staining, immunofluorescence, transmission electron microscopy, ALP/ARS staining, and dual-luciferase assay were used to detect related indicators. Results showed TNF-α downregulated miR-335-5p, upregulated DKK1, inhibited autophagy, induced senescence, disrupted cytoskeleton, and suppressed osteogenesis; miR-335-5p directly targeted DKK1's 3'-UTR. Overexpressing miR-335-5p or silencing DKK1 restored DPSCs' autophagic flux, alleviated senescence, and rescued osteogenic potential. In conclusion, the miR-335-5p/DKK1/autophagy axis mediates TNF-α-induced DPSCs dysfunction, and targeting this axis may improve stem cell-based dental pulp and bone reconstruction under inflammation.
Indexed as
Identifiers
42496832What 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.