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Clinical Implications of Basic Research
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Volume 360:1567-1569 April 9, 2009 Number 15
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Limiting Fibrosis after Myocardial Infarction
Bodh I. Jugdutt, M.D., D.M.

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A recent study by Kobayashi and colleagues1 showed that a secreted protein may be a therapeutic target for limiting fibrosis and improving function after myocardial infarction. Myocardial infarction is a catastrophic event, causing damage to the heart wall — usually, the wall of the left ventricular chamber, which pumps blood into the circulation to perfuse other vital organs. This can lead to heart failure and, consequently, to disability or death. The wound, caused by necrosis and apoptosis after coronary-artery occlusion, triggers the healing process, resulting in a strong fibrotic scar and the restoration of pump function.

Healing is accomplished through . . . [Full Text of this Article]


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From the Division of Cardiology, Department of Medicine and Cardiovascular Research Group, Faculty of Medicine, University of Alberta, Edmonton, Canada.



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