ArticleMolecular medicine reports2017
Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- New opportunities to overcome T cell dysfunction: the role of transcription factors and how to target them.Trends in biochemical sciences · 2024Review
- Searching for Effective Treatments in HFpEF: Implications for Modeling the Disease in Rodents.Pharmaceuticals (Basel, Switzerland) · 2023Review
- How does NFAT3 regulate the occurrence of cardiac hypertrophy?International journal of cardiology. Heart & vasculature · 2023Review
- Synthesis, Biosynthesis, and Biological Activity of Diels-Alder Adducts fromMolecules (Basel, Switzerland) · 2022Review
- Mulberry Diels-Alder-type adducts: isolation, structure, bioactivity, and synthesis.Natural products and bioprospecting · 2022Review
- Sanggenon C Ameliorates Cerebral Ischemia-Reperfusion Injury by Inhibiting Inflammation and Oxidative Stress through Regulating RhoA-ROCK Signaling.Inflammation · 2020Article
- Sanggenon C Stimulates Osteoblastic Proliferation and Differentiation, Inhibits Osteoclastic Resorption, and Ameliorates Prednisone-Induced Osteoporosis in Zebrafish Model.Molecules (Basel, Switzerland) · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of Sanggenon C on oxidative stress and inflammation have previously been reported; however, little is currently known regarding the effects of Sanggenon C on cardiac hypertrophy and fibrosis. In the present study, aortic banding (AB) was performed on mice to induce cardiac hypertrophy. After 1 week AB surgery, mice were treated daily with 10 or 20 mg/kg Sanggenon C for 3 weeks. Subsequently, cardiac function was detected using echocardiography and catheter‑based measurements of hemodynamic parameters. In addition, the extent of cardiac hypertrophy was evaluated by pathological staining and molecular analysis of heart tissue in each group. After 4 weeks of AB, vehicle‑treated mice exhibited cardiac hypertrophy, fibrosis, and deteriorated systolic and diastolic function, whereas treatment with 10 and 20 mg/kg Sanggenon C treatment ameliorated these alterations, as evidenced by attenuated cardiac hypertrophy and fibrosis, and preserved cardiac function. Furthermore, AB‑induced activation of calcineurin and nuclear factor of activated T cells 2 (NFAT2) was reduced following Sanggenon C treatment. These results suggest that Sanggenon C may exert protective effects against cardiac hypertrophy and fibrosis via suppression of the calcineurin/NFAT2 pathway.
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Registered trials
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