ArticleInflammation2026
IL-17-associated Pro-inflammatory Programs in Aortic Valve Interstitial Cell Osteogenic Differentiation: JUN as a Candidate Regulator.
Article in Inflammation, 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
12 authors.
Funding
Abstract
Calcific aortic valve disease (CAVD) involves fibro-calcific remodeling, in which osteogenic differentiation of valvular interstitial cells (VICs) is a key process. Although inflammation is implicated, uncertainties persist regarding how defined pro-inflammatory pathways are transcriptionally coupled to the VIC osteogenic program at the cell-intrinsic level. We implemented an interleukin-17 (IL-17) pathway-guided transcriptomic strategy in a pure human VIC osteogenic differentiation model. RNA sequencing identified osteogenesis-associated differentially expressed genes and IL-17-related inflammatory signatures. Functional enrichment and multilayer network analyses were applied to prioritize candidate regulatory nodes, followed by in vitro validation. An IL-17-associated transcriptional program was activated during VIC osteogenic differentiation and was enriched for stress-activated and MAPK-related inflammatory pathways. Network-based analyses consistently identified the AP-1 transcription factor JUN as a central regulatory node within this IL-17-linked signature. Experimentally, JUN expression increased during VIC osteogenic differentiation, and JUN silencing attenuated calcification. IL-17 A rapidly increased the p-c-JUN/JUN ratio, and prolonged treatment upregulated JUN and IL-17RA in a concentration-dependent manner. Exogenous IL-17 A stimulation enhanced calcification-related phenotypes in VICs, which were partially reversed by JUN knockdown. In a chronic kidney disease-induced mouse CAVD model, JNK inhibition with SP600125 reduced valve calcification and leaflet thickness. IL-17-associated inflammatory signaling is engaged during VIC osteogenic differentiation and may promote calcification, partially through a JUN-dependent mechanism. These findings provide insight into how inflammatory programs interface with osteogenic transcription and offer a framework for dissecting inflammation-driven calcification in CAVD.
Indexed as
Identifiers
42479100What 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.