ArticleHuman cell2025
Apigenin inhibits endothelial-to-mesenchymal transition of coronary artery endothelial cells and myocardial fibrosis by regulating ribosome biogenesis through GTPBP4 modulation.
Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Novel susceptibility genes for varicose veins revealed by a cross-tissue transcriptome-wide association study.Science progressArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Myocardial fibrosis is a complex pathological process that often leads to myocardial dysfunction, heart failure, and ultimately, death. A critical contributor to the development of cardiac fibrosis is the endothelial-to-mesenchymal transition (EndMT). Apigenin, a natural compound derived from Matricaria chamomilla, has shown potential anti-fibrotic effects, although its precise mechanism of action is not fully understood. This study investigated the effects of apigenin (API) on EndMT and myocardial fibrosis using an in vitro human coronary artery endothelial cell EndMT model and an in vivo animal model of fibrosis. At appropriate concentrations, apigenin significantly inhibited TGF-β1-induced EndMT and myocardial fibrosis without affecting cell viability. Mechanistically, we found that apigenin suppressed ribosome biogenesis in coronary endothelial cells. Through differential gene screening, GTP-binding protein 4 (GTPBP4) was identified as a key target gene regulating ribosome biogenesis during the progression of myocardial fibrosis. Our results indicate that GTPBP4 plays a pivotal role in the apigenin-mediated inhibition of both ribosome biogenesis and EndMT in these cells. By downregulating GTPBP4 expression, apigenin suppressed EndMT, alleviated myocardial fibrosis, improved cardiac function, and reduced biomarkers of myocardial injury. These findings demonstrate for the first time that apigenin mitigates myocardial fibrosis and EndMT by inhibiting GTPBP4 expression, positioning apigenin as a promising therapeutic candidate for the prevention and treatment of myocardial fibrosis.
Indexed as
Identifiers
40938540What 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.