ArticleBalkan medical journal2026
Overexpression of Circ_0004496 is Associated with Pathological Bone Formation in Ankylosing Spondylitis via the miR-145/ACTG1 Axis.
Article in Balkan medical journal, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The functional role of circular ribonucleic acids in ankylosing spondylitis (AS) remains poorly understood. In our previous study, circ_0004496 and actin gamma 1 (ACTG1) were found to be upregulated in ossified tissues from patients with AS. Aims: To investiagate the regulatory role of circ_0004496 in pathological bone formation through the miR-145/ACTG1 axis. Study Design: Combined Methods: Tissue samples were obtained from 15 patients with AS and hip ankylosis and 15 control patients with femoral neck fractures. Quantitative real-time polymerase chain reaction was performed to measure circ_0004496 and miR-145 expression. Western blot analysis was used to determine the protein levels of alkaline phosphatase (ALP), osteocalcin (OCN), runt-related transcription factor 2 (Runx2), and ACTG1. Cell proliferation was evaluated using Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine assays. Osteogenic differentiation was assessed by measuring ALP activity and performing Alizarin Red S staining. Interactions among circ_0004496, miR-145, and ACTG1 were examined using RNA immunoprecipitation (RIP), RNA pull-down, dual-luciferase reporter, and fluorescence Results: Circ_0004496 and ACTG1 expression levels were significantly elevated in AS hip capsule tissues, whereas miR-145 expression was reduced. Overexpression of circ_0004496 in AS-derived fibroblasts enhanced cell proliferation, accelerated cell cycle progression, increased calcium deposition, and upregulated ALP, OCN, and Runx2 protein levels. Mechanistically, circ_0004496 functioned as a molecular sponge for miR-145, which directly targets ACTG1. These regulatory interactions were confirmed by dual-luciferase reporter, RIP, RNA pulldown, and FISH assays. Conclusion: Circ_0004496 overexpression promotes pathological bone formation in AS by regulating the miR-145/ACTG1 axis both
Indexed as
Identifiers
What Socratic 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 Socratic graph.