Extracellular Matrix Proteomics in Cardiac Ischemia/Reperfusion: The Search is On
Prolonged myocardial ischemia leads to myocytenecrosis, which initiates a localized inflammatory response that catabolizes the cellular debris and initiates deposition of extracellular matrix (ECM) proteins.1 In addition to providing a vital structural framework for the three-dimensional organization of cells, the ECM determines the physical properties of biological tissues and acts as a dynamic microenvironment for cellular signaling. A number of cardiac diseases, including myocardial ischemia and reperfusion (I/R), are associated with qualitative and quantitative alterations in ECM proteins.2 Understanding ECM changes is important for identifying factors that tip the balance between favorable reparative remodeling following myonecrosis and adverse remodeling that leads to progressive ventricular dilatation and congestive heart failure.(SELECT FULL TEXT TO CONTINUE)
- Received January 8, 2012.
- Accepted January 13, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited