ArticleJournal of molecular histology2025
CircZNF418 alleviates oxidative stress-induced cartilage endplate degeneration by stabilizing Sox9 through HuR.
Article in Journal of molecular histology, 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
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
1 citing paper in PubMed.
- Resetting the epigenetic clock: cellular senescence and regenerative strategies in intervertebral disc degeneration.Frontiers in aging · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Intervertebral disc degeneration (IDD) significantly contributes to back pain, impacting patients' quality of life, and the cartilaginous endplate (CEP) is crucial to the functioning of the disc in both normal and disease states. Furthermore, circular RNAs (circRNAs) have been implicated in the modulation of a variety of diseases, including IDD. Nonetheless, the specific involvement of circRNAs in the the intervertebral disc CEP degeneration is not yet fully understood. The objective of this research was to explore the function and potential mechanism of circZNF418 in the context of CEP degeneration. We employed Western blotting, immunofluorescence, and qRT-PCR to evaluate the expression levels of circZNF418, its binding protein human antigen R (HuR), and Sox9. The cell counting Kit-8 (CCK-8) assay was employed to assess the functional impact of circZNF418 on cell viability. Bioinformatics analysis was conducted to identify the interaction between the RNA-binding protein HuR and circZNF418. Our findings indicated that the levels of expression for both circZNF418 and Sox9 were notably reduced in degenerative CEP cells, as well as in CEP cells subjected to oxidative stress. Furthermore, oxidative stress was found to decrease cell viability in CEP cells, reduce the expression of extracellular matrix (ECM)-related proteins (collagen II and aggrecan), and increase the levels of matrix metalloproteinases (MMP3 and MMP13). Notably, overexpression of circZNF418 mitigated these oxidative stress-induced effects. CircZNF418 overexpression also significantly enhanced the proliferation of CEP cells. Additionally, the overexpression of circZNF418 resulted in an increase in Sox9 mRNA and protein levels, while simultaneously decreasing the protein levels of MMP3 and MMP13, and increasing those of collagen II and aggrecan. We found that circZNF418 promotes the expression and protein translation of the downstream gene Sox9 by interacting with HuR. Conversely, interference with Sox9 reversed the inhibitory effects of circZNF418 on oxidative stress-induced degeneration of CEP cells. In conclusion, circZNF418 alleviates the degeneration of CEP cells caused by oxidative stress by stabilizing Sox9 through HuR interaction. Therefore, a deeper exploration of its molecular mechanism is crucial for advancing the prevention and treatment of IDD.
Indexed as
Identifiers
40742571What 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.