Enzyme Has Key Role in Heart Disease

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British researchers have discovered that an enzyme called matrix metalloproteinase-8 (MMP8) is a key player in the accumulation of plaque in the arteries, which increases the risk of heart disease. This new finding could help scientists eventually develop new ways to treat and prevent heart disease.

The enzyme MMP8, which is also known as collagenase-3 or neutrophil collagenase, is known to cause inflammation, which in recent years has been identified as a risk factor for heart disease. Therefore gaining a better understanding of how MMP8 contributes to heart disease could lead to some significant developments in the fight against this number one killer of adults in the United States, the United Kingdom, and many other countries throughout the world.

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In this new study, the researchers studied mice that had been genetically modified so they could not produce the MMP8 enzyme. The mice were then fed a diet high in fat and cholesterol (a Western-style diet) and compared with mice that had not been altered and who were fed the same diet. The mice that did not have the enzyme had lower blood pressure and less plaque in their arteries.

In addition to the mouse study, the researchers also evaluated 2,000 patients who were undergoing a coronary angiogram to test for blockages in their arteries. Approximately one-quarter of the patients had a slightly different version of the gene for MMP8 and their arteries were more clogged than those in other patients who had a normal version of the gene.

Angiotension-converting enzyme (ACE) inhibitors are among the most popular drugs used to treat high blood pressure, congestive heart failure, and people who have had a heart attack. Some of these individuals do not respond well or sufficiently to ACE inhibitors alone, and so they need other treatment options that can enhance the ACE inhibitor effect or offer protection against heart disease in other ways. Scientists hope continued research on MMP8 will uncover new ways to prevent and treat heart disease.

SOURCES:
Laxton RC et al. Circulation Research 2009; September DOI: 10.1161/CIRCRESAHA.109.200279
Van Lint P, Libert C. Cytokine Growth Factor Review 2006 Aug; 17(4): 217-23

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