ArticleFrontiers in pharmacology2026
Naringenin inhibited vascular calcification and attenuated senescence-associated changes through the p53/TOP2Aaxis.
Article in Frontiers in pharmacology, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Vascular calcification (VC) is a major cardiovascular complication of chronic kidney disease (CKD). Senescence-associated vascular changes have been increasingly implicated in CKD-related VC. Naringenin, a natural flavonoid with anti-oxidative and anti-inflammatory properties, has shown protective effects in several age-related disorders, but its role and mechanism in CKD-associated VC remain unclear. Methods: Human vascular specimens, high-Pi-induced vascular smooth muscle cells (VSMCs), and an adenine/high-phosphate-induced rat model of CKD-associated VC were used to evaluate the relationship between calcification and senescence-associated changes and to assess the effects of naringenin. Histological staining, SA-β-Gal staining, Western blotting, immunofluorescence, immunohistochemistry, RNA sequencing, molecular docking, chromatin immunoprecipitation, and dual-luciferase assays were performed to explore the possible mechanism. Results: VC was positively associated with senescence-associated changes in patient tissues, cultured VSMCs, and rat aortas. Naringenin significantly reduced calcium deposition and attenuated senescence-associated marker changes both Conclusion: Naringenin inhibits vascular calcification by modulating the p53/TOP2A axis, and this protective effect is accompanied by attenuation of senescence-associated changes. These findings support naringenin as a mechanistically relevant candidate for CKD-associated vascular calcification, although the upstream mechanism underlying p53 suppression remains to be clarified.
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.