ArticleJournal of thoracic disease2025
Circular RNA circFTO promotes pressure overload-induced cardiac hypertrophy by encoding a novel protein FTO-36aa.
Article in Journal of thoracic disease, 2025. 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: Pathological cardiac hypertrophy leading to ventricular remodeling poses a significant threat to human health. Circular RNAs (circRNAs) play a potential role in the dysregulation of cardiac hypertrophy, and recent evidence highlights their translational ability in various diseases. However, it is not clear whether circRNAs play a protein-coding role in myocardial hypertrophy and ventricular remodeling. This study aimed to investigate the role of circRNA derived from the fat mass and obesity-associated ( Methods: A transverse aortic constriction (TAC)-induced hypertrophy mouse model was established. The heart function of the C57BL/6 mice was evaluated. Myocardial structure injury and fibrosis were analyzed by hematoxylin and eosin (H&E) staining and Masson staining. CircRNA microarray assays were used to screen the dysregulated circRNAs. The recombinant adenovirus-associated virus (AAV) was constructed to overexpress or knockdown FTO protein or circFTO. Mass spectrometry analyses, dual-luciferase reporter assays, and polysome profiling analyses were performed to detect the FTO-36aa. Results: The study identified dysregulated circRNAs in sham and TAC models, and found that an upregulated circRNA, circFTO, is generated from the back-splicing of FTO exon 5 and exon 7. The silencing of circFTO by AAV significantly weakened the TAC-induced hypertrophy phenotype. The study also identified a novel protein, FTO-36aa, coded by circFTO, that caused the pro-hypertrophy effect of circFTO. FTO-36aa promoted the ubiquitination-mediated protein degradation of FTO, which suppressed the demethylation of RNA, elevating the global N6-methyladenosine (m Conclusions: Overall, this study shed light on the functional importance of alternative splicing-generated circFTO and its coded FTO-36aa during myocardial hypertrophy. The findings provide fundamental insights into the mechanisms of m
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.