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Ann Thorac Surg 2007;84:133
© 2007 The Society of Thoracic Surgeons


Original Articles: Cardiovascular

Invited commentary

David J. Chambers, PhD

Cardiac Surgical Research, The Rayne Institute (King’s College London), Guy’s and St. Thomas’ NHS Foundation Trust, St. Thomas’ Hospital, London, SE1 7EH United Kingdom

(Email: david.chambers@kcl.ac.uk).

The first 20% of the full text of this article appears below.

The article by Barillas and colleagues [1] is the latest in an elegant series of studies from this group relating to the effects of ischemia-reperfusion on hypertrophied hearts. The study was conducted on neonatal rabbits that were subjected to aortic banding for 6 weeks to achieve early decompensated hypertrophy, which was shown to reduce tolerance to ischemia-reperfusion. This reduced tolerance is associated with impairment in insulin-induced glucose uptake and seems to be linked to defects in insulin signaling pathway (rather than in glucose transport). The authors hypothesize that glucose synthase kinase-3ß (GSK-3ß; a key intermediate in this pathway) has become activated due to a reciprocal reduction in activity of the . . . [Full Text of this Article]


Related Article

Inhibition of Glycogen Synthase Kinase-3ß Improves Tolerance to Ischemia in Hypertrophied Hearts
Rodrigo Barillas, Ingeborg Friehs, Hung Cao-Danh, Joseph F. Martinez, and Pedro J. del Nido
Ann. Thorac. Surg. 2007 84: 126-133. [Abstract] [Full Text] [PDF]






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