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Reducing the damage of a heart attack
Date:12/15/2008

d improved recovery to their heart function, which leads the authors to believe that the protein has a direct affect on muscle scarring and stiffening following myocardial infarction.

The Weill Cornell team collaborated with Dr. Daniel S. Greenspan, co-senior author and professor of pathology and laboratory medicine from the University of Wisconsin School of Medicine and Public Health in Madison, Wis. Dr. Greenspan determined how the main component of connective tissue, collagen, interacts with the sFRP2 protein, and how these molecules play a crucial role in scar formation.

"With many injuries and diseases, large amounts of collagen are formed and deposited in tissues, leading to scarring and fibrosis," says Dr. Greenspan, an expert in collagen. "Fibrosis can severely affect the functioning of the heart, lung, liver and other tissues."

Together, the researchers determined that the sFRP2 protein works by accelerating the processing of pro-collagen, a precursor of mature collagen, the main component deposited in scar tissue. Following a heart attack, fibrous collagen deposits are increased, replacing the dead muscle and leading to more scar tissue, which prevents recovery.

"Therapeutically, the findings mean that it is possible to create a drug that may one day inhibit the functioning of the protein in order to limit fibrosis within the heart," says Dr. Sato. "Doing so may aid in controlling the degree of scarring, and allow the heart to continue to function following myocardial infarction."


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Contact: Andrew Klein
ank2017@med.cornell.edu
212-821-0560
New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College
Source:Eurekalert

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