ArticleFrontiers in pharmacology2020
Effect of Triptolide on Temporal Expression of Cell Cycle Regulators During Cardiac Hypertrophy.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 5 citations in OpenAlex.
- C-C motif receptor 2 is a core profibrotic factor in uremic cardiomyopathy.Disease models & mechanisms · 2026Article
- Diverging targets mediate the pathological roleof miR-199a-5p and miR-199a-3p by promoting cardiac hypertrophy and fibrosis.Molecular therapy. Nucleic acids · 2021Article
- miR-199a Overexpression Enhances the Potency of Human Induced-Pluripotent Stem-Cell-Derived Cardiomyocytes for Myocardial Repair.Frontiers in pharmacology · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Adult mammalian cardiomyocytes may reenter the cell cycle and cause cardiac hypertrophy. Triptolide (TP) can regulate the expressions of various cell cycle regulators in cancer cells. However, its effects on cell cycle regulators during myocardial hypertrophy and mechanism are unclear. This study was designed to explore the profile of cell cycle of cardiomyocytes and the temporal expression of their regulators during cardiac hypertrophy, as well as the effects of TP. The hypertrophy models employed were neonatal rat ventricular myocytes (NRVMs) stimulated with angiotensin II (Ang II) for scheduled times (from 5 min to 48 h)
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