Key result
Atorvastatin prevented cellular energy metabolism switching from oxidative phosphorylation to glycolysis induced by angiotensin II and protected the proliferative ability of human umbilical vein endothelial cells.
Why the study?
Does atorvastatin prevent angiotensin II-induced inhibition of proliferation and mitochondrial energy metabolism changes in human umbilical vein endothelial cells?
Population
Human umbilical vein endothelial cells (HUVECs) cultured in vitro
Comparison
10 µM atorvastatin combined with 1 µM… vs 1 µM angiotensin II alone and untreated control
Design
Preclinical
Follow-up
24 hours
Authors
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May protect endothelial cells in vitro; leaves open clinical translation in cardiovascular disease.
Does atorvastatin prevent angiotensin II-induced inhibition of proliferation and mitochondrial energy metabolism changes in human umbilical vein endothelial cells?
Atorvastatin protects endothelial cell proliferation against angiotensin II-induced inhibition by preserving mitochondrial oxidative phosphorylation and preventing a switch to glycolysis.
Ye et al. (2017) studied Angiotensin II-induced endothelial dysfunction. Atorvastatin vs. Angiotensin II alone or control was evaluated on Cell proliferation and mitochondrial energy metabolism. Atorvastatin prevented cellular energy metabolism switching from oxidative phosphorylation to glycolysis induced by angiotensin II and protected the proliferative ability of human umbilical vein endothelial cells.
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