Prostaglandin E2 in Remote Control of Myocardial Remodeling
Despite the advance in treatment of acute myocardial infarction (MI) with timely reperfusion of ischemic myocardium, coronary artery disease remains a leading cause of morbidity and mortality worldwide. In patients survived acute MI, heart undergoes a remodeling process characterized by changing in size, shape, structure, and function. The progressive ventricular dilation, wall thinning, fibrosis, together with loss of contractile function lead to life-threatening heart failure and arrhythmia. Therefore understanding the process of pathological remodeling in post-MI hearts is of paramount importance.
It is well established that inflammatory response is elicited by MI and contributes significantly to cardiac remodeling. At the onset of MI injury, inflammatory leukocytes produced in bone marrow are mobilized and infiltrate the myocardium from circulation. The locally targeted leukocytes can be beneficial to wound healing by removing dead cells and matrix debris. However, prolonged inflammation may also contribute to additional cell death and scar formation due to fibrosis. Therefore inflammatory response has to be precisely controlled and timely resolved to avoid adverse remodeling in the post-infarct heart 1,2. As a result, modulating inflammatory response has been considered a potential therapeutic approach to preserve and recover heart function after MI 3,4. A great deal of effort has been made to understand the cellular and molecular mechanisms of inflammatory response following MI 2,5-8. (SELECT FULL TEXT TO CONTINUE)
- Received May 1, 2012.
- Accepted May 3, 2012.
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