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Putting energy into heart protection

Under conditions of stress, molecular mechanisms stop cells from consuming their source of energy, ATP, and trigger them to begin to produce ATP. This is done by inducing cells to stop any biochemical pathways that use energy and by turning on processes that take up glucose and free fatty acids from their surroundings in order to rebuild their ATP reservoir. The main protein involved in this switch is called AMP-activated protein kinase (AMPK). One situation of obvious energy stress on cells is during a heart attack. Lawrence Young and colleagues at Yale University School of Medicine, have now investigated the biological importance of AMPK during heart trauma in mice, and find that AMPK is vital for protecting cells under conditions of a heart attack. The authors used a transgenic mouse that had an inactivated AMPK and found that under normal circumstances the hearts of these mice and those of wild-type mice were generally similar in form and function. These mutant mice did have slightly lower diastolic pressure in the left ventrical. Upon reduction of blood flow to the heart, to simulate a heart attack, they found that the mice without a functioning AMPK could not stimulate glucose uptake, although the molecular mechanisms for glucose uptake were intact, nor did they breakdown fatty acids to replenish ATP. Once blood flow returned, contractile function in the left ventrical of the mutant mice was impaired. The authors found that there was an increased amount of cell death in these tissues, both through necrosis and programmed cell death, called apoptosis. These data indicate that AMPK is responsible for altering cellular mechanisms for energy in the heart and plays an important protective role during and after a heart attack. The identification of novel AMPK targets and/or the possible use of AMPK activators may be useful in providing therapy for healing during or after a heart attack.

A related commentary in this issue by D. Grahame Hardy from th
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Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
16-Aug-2004


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