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      Protective Effect of Spironolactone on Endothelial-to-Mesenchymal Transition in HUVECs via Notch Pathway.

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          Abstract

          Fibrosis results in excessive buildup of extracellular matrix proteins along with abnormalities in structure and is partly derived by a process involving transforming growth factor β (TGF-β) called endothelial-to-mesenchymal transition (EndMT). We investigated whether the aldosterone receptor-blocker spironolactone could abrogate TGF-β-induced fibrosis in EndMT and the underlying mechanism.

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          Author and article information

          Journal
          Cell. Physiol. Biochem.
          Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
          S. Karger AG
          1421-9778
          1015-8987
          2015
          : 36
          : 1
          Affiliations
          [1 ] Department of Cardiology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
          Article
          000374063
          10.1159/000374063
          25967959

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