Key result
Antagonism of miR-21 attenuated TGF-β-mediated endothelial-to-mesenchymal transition via the PTEN/Akt pathway in vitro and in mice subjected to left ventricular pressure overload.
Why the study?
Does miR-21 antagonism prevent TGF-β-induced endothelial-to-mesenchymal transition in cardiac fibrosis models?
Population
Endothelial cells (in vitro) and mice subjected to left ventricular pressure overload (in vivo)
Design
Preclinical
Authors
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miR-21 antagonism may mitigate fibrosis in pressure overload; hypothesis-generating for therapeutic translation in human heart failure.
Does miR-21 antagonism prevent TGF-β-induced endothelial-to-mesenchymal transition in cardiac fibrosis models?
Antifibrotic effects of miR-21 antagonism are partly mediated by blocking endothelial-to-mesenchymal transition under stress conditions.
Kumarswamy et al. (2011) studied Cardiac fibrosis. miR-21 antagonism was evaluated on Endothelial-to-mesenchymal transition. Antagonism of miR-21 attenuated TGF-β-mediated endothelial-to-mesenchymal transition via the PTEN/Akt pathway in vitro and in mice subjected to left ventricular pressure overload.
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