2-5-dimethylcelecoxib has been researched along with Cardiomegaly* in 2 studies
2 other study(ies) available for 2-5-dimethylcelecoxib and Cardiomegaly
| Article | Year |
|---|---|
2,5-Dimethylcelecoxib prevents isoprenaline-induced cardiomyocyte hypertrophy and cardiac fibroblast activation by inhibiting Akt-mediated GSK-3 phosphorylation.
We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative that is unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3) and prolonged the lifespan of heart failure mice with genetic dilated cardiomyopathy or transverse aortic constriction-induced left ventricular hypertrophy. However, it remained unclear how DM-celecoxib regulated structure and function of cardiomyocytes and cardiac fibroblasts involved in cardiac remodeling. In the present study, therefore, we investigated the effect of DM-celecoxib on isoprenaline-induced cardiomyocyte hypertrophy and cardiac fibroblast activation, because DM-celecoxib prevented isoprenaline-induced cardiac remodeling in vivo. DM-celecoxib suppressed isoprenaline-induced neonatal rat cardiomyocyte hypertrophy by the inhibition of Akt phosphorylation resulting in the activation of GSK-3 and the inhibition of β-catenin and mammalian target of rapamycin (mTOR). DM-celecoxib also suppressed the proliferation and the production of matrix metalloproteinase-2 and fibronectin of rat cardiac fibroblasts. Moreover, we found that phosphatase and tensin homolog on chromosome 10 (PTEN) could be a molecule to mediate the effect of DM-celecoxib on Akt. These results suggest that DM-celecoxib directly improves the structure and function of cardiomyocytes and cardiac fibroblasts and that this compound could be clinically useful for the treatment of β-adrenergic receptor-mediated maladaptive cardiac remodeling. Topics: Animals; Animals, Newborn; Cardiomegaly; Disease Models, Animal; Fibroblasts; Glycogen Synthase Kinase 3; Isoproterenol; Male; Mice; Mice, Inbred C57BL; Myocytes, Cardiac; Phosphorylation; Proto-Oncogene Proteins c-akt; Pyrazoles; Rats; Rats, Sprague-Dawley; Sulfonamides; Ventricular Remodeling | 2019 |
2,5-Dimethylcelecoxib prevents pressure-induced left ventricular remodeling through GSK-3 activation.
Topics: Animals; Cardiomegaly; Cardiomyopathy, Dilated; Disease Models, Animal; Glycogen Synthase Kinase 3; Heart Ventricles; Matrix Metalloproteinase 2; Mice; Mice, Knockout; Proto-Oncogene Proteins c-akt; Pyrazoles; Sulfonamides; Ventricular Remodeling | 2017 |