Background: Glutaredoxin-1 (Glrx) inhibits endothelial cell migration by reversing protein-glutathione adducts. Results: Revascularization after hind limb ischemia was inhibited in Glrx transgenic mice. Glrx overexpression increased soluble VEGF receptor 1 (sFlt) in endothelial cells via NF-B-dependent Wnt5a production. Conclusion: Glrx enhances Wnt5a-induced anti-angiogenic sFlt in endothelial cells. Significance: Up-regulated Glrx inhibits VEGF signaling by increased sFlt causing impaired vascularization.

Klinefelter syndrome can present as a wide spectrum of clinical manifestations at various stages in life, making it a chromosomal disorder with no standardized set of guidelines for appropriate management. Understanding the genetic and hormonal causes of this syndrome can allow physicians to treat each patient on a more individualized basis. The timing of diagnosis and degree of symptoms can guide management. This report will provide an updated review of the clinical presentation at various stages in life and the implications for management.

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