Akt is a molecule involved in many cellular functions, including growth, survival, and metabolism. Akt exists in three isoforms Akt1, Akt2, and Akt3, which have a substantial degree of functional overlap. In the heart and vasculature, Akt may be protective against ischemia and it may enhance cardiac function after heart failure. But Akt may also have detrimental effects.

In our August 1 issue, the Journal of Clinical Investigation presents three research papers that explore Akt1 in the heart, plus an accompanying commentary. The first paper, by Anthony Rosenzweig and colleagues at Harvard, and the second paper by Kenneth Walsh and colleagues at Boston University, both provide new insights into how Akt1 can be maladaptive in the heart. Both studies use transgenic mice that overexpress active Akt1 to show that this causes cardiac dysfunction, including hypertrophy and fibrosis.

The third paper in this issue, by William Sessa and colleagues at Yale University, explores which Akt isoform is responsible for mediating adaptive angiogenesis seen in the heart after ischemia. The authors find that Akt1, but not Akt2 or Akt3 is responsible.

In an accompanying commentary that discusses all three papers, Brian O'Neill and E. Dale Abel write, "Three separate studies published in this issue of the JCI now provide important new insight into the central role of Akt1 in the regulation of angiogenesis and the maladaptive or deleterious consequences of chronic unregulated Akt activation in the heart." They proceed to discuss the implications of this data.

TITLE 1: Phosphoinositide 3-kinase rescues the detrimental effects of chronic Akt activation in the heart during ischemia/reperfusion injury

AUTHOR CONTACT 1:
Anthony Rosenzweig
Massachusetts General Hospital, Charlestown, MA USA
Phone: 617-726-8286; Fax
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Contact: Stacie Bloom
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
1-Aug-2005