Title : Androgen attenuates cardiac fibroblasts activations through modulations of transforming growth factor-β and angiotensin II signaling.

Pub. Date : 2014 Sep 20

PMID : 25125004






3 Functional Relationships(s)
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1 Testosterone-treated fibroblasts had decreased phosphorylated Akt, mammalian target of rapamycin, and 4E binding protein-1 irrespective of TGF-beta1 treatment and had increased matrix metalloproteinase (MMP)-2 in the presence of TGF-beta1 treatment, and had decreased phosphorylated P38 and Smad 2/3 levels in the presence of Ang II. Testosterone AKT serine/threonine kinase 1 Homo sapiens
2 Cardiac fibroblasts with and without testosterone had similar mRNA and protein expressions of total Akt and total Smad 2/3 irrespective of TGF-beta1 or Ang II treatment. Testosterone AKT serine/threonine kinase 1 Homo sapiens
3 CONCLUSION: Physiological level of testosterone attenuated Akt and Smad 2/3 phosphorylation mediated by TGF-beta1 and angiotensin II respectively, which can result in decreased cardiac fibroblast activation and potentially contribute to beneficial effects in heart failure. Testosterone AKT serine/threonine kinase 1 Homo sapiens