ArticleFrontiers in pharmacology2022
Disturbing effect of cepharanthine on valve interstitial cells calcification
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Decoding the lactylation-immune link in calcific aortic valve disease: a comprehensive bioinformatics approach.Human genomics · 2025Article
- Article
- Morusin Alleviates Aortic Valve Calcification by Inhibiting Valve Interstitial Cell Senescence Through Ccnd1/Trim25/Nrf2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role of glycolysis in inflammatory bowel disease and its associated colorectal cancer.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteogenic differentiation of valve interstitial cells (VICs) directly leads to aortic valve calcification, which is a common cardiovascular disease caused by inflammation and metabolic disorder. There is still no ideal drug for its treatment and prevention. The purpose of this study was to explore the effect and molecular mechanism of cepharanthine (CEP), a natural product, on inhibiting the osteogenic differentiation of VICs. First, CCK8 assay was used to evaluate cell viability of CEP on VICs. CEP concentration of 10 μM was the effective dose with slight cytotoxicity, which was used for further study. The alizarin red staining analysis showed that CEP significantly inhibited calcium deposition caused by osteogenic medium related calcification induction. In order to explore the anti-calcification molecular mechanism of CEP, transcriptome and metabolome were synchronously used to discover the possible molecular mechanism and target of CEP. The results showed that CEP inhibited valve calcification by regulating the glycolytic pathway. The molecular docking of CEP and selected key factors in glycolysis showed significant binding energies for GLUT1 (-11.3 kcal/mol), ENO1 (-10.6 kcal/mol), PKM (-9.8 kcal/mol), HK2 (-9.2 kcal/mol), PFKM (-9.0 kcal/mol), and PFKP (-8.9 kcal/mol). The correlation analysis of RUNX2 expression and cellular lactate content showed R
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