Key result
Delphinidin significantly attenuated pathological cardiac hypertrophy and fibrosis in vivo and in vitro by modulating oxidative stress through the AMPK/NOX/MAPK signaling pathway.
Delphinidin attenuates pathological cardiac hypertrophy by modulating oxidative stress via the AMPK/NOX/MAPK signaling pathway in preclinical models.
No takes yet. Share an insight, caveat, or question.
Should not yet change clinical practice; hypothesis-generating for AMPK-targeted therapies in cardiac remodeling.
Chen et al. (2020) studied Pathological cardiac hypertrophy. Delphinidin vs. DMSO (vehicle) was evaluated on Cardiac hypertrophy and fibrosis (HW/BW, HW/TL, cardiomyocyte size). Delphinidin significantly attenuated pathological cardiac hypertrophy and fibrosis in vivo and in vitro by modulating oxidative stress through the AMPK/NOX/MAPK signaling pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: