Editors' ChoiceCardiovascular Disease

A New Trick of the Light: Saving the Heart from Ischemia

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Science Translational Medicine  27 Jun 2012:
Vol. 4, Issue 140, pp. 140ec111
DOI: 10.1126/scitranslmed.3004506

When a heart attack strikes, the muscle of the heart becomes ischemic—lacking nutrients and oxygen as a result of blood flow blockage. In the critical window after a heart attack, heart cells must fight to survive until blood flow can be restored. Few nonsurgical options exist for intervention. Now, Eckle et al. have discovered that something as simple as exposure to intense light for a few hours may dramatically reduce the damage from a heart attack.

In ischemic heart disease, adenosine signaling acts as a metabolic switch to allow heart cells to adapt to the lack of oxygen and nutrients by changing from an “energy-efficient” mode to an “oxygen-efficient” state. This switch helps heart cells to survive the ischemic conditions and recover normal function after a heart attack. Adenosine concentrations increase during ischemia, activating a family of adenosine receptors.

Eckle and colleagues examined samples from hearts of patients with ischemic heart disease, finding more adenosine receptor A2b (Adora2b) in diseased hearts than in healthy hearts. They then created a mouse that lacked Adora2b and used microarray analysis to identify the gene with the greatest change due to Adora2b loss: Period 2 (Per2), a circadian rhythm protein. Mice in which Per2 had been knocked out showed larger regions of damage to the heart muscle after a heart attack. The authors went on to show that Per2 could be induced by exposure to light in normal mice, and the induction of this protein resulted in less heart damage from heart attack.

The new work of Eckle et al. suggests that treatment with intense light may limit the damage to heart muscle during a heart attack. If their results apply to humans, they suggest an eminently translatable and inexpensive treatment—light exposure.

T. Eckle et al., Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia. Nat. Med. 18, 774–782 (2012). [Abstract]

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