health-news

Gene therapy set to become future of heart disease treatment

Washington, Oct. 7 : A global hunt for genes influencing heart disease risk has uncovered 157 changes in human DNA that alter levels of cholesterol and other blood fats - a finding that may lead to new medications.


Each of the changes points to genes that can modify levels of cholesterol and other blood fats and are potential drug targets. Many of the changes point to genes not previously linked to blood fats, also called lipids.

A surprising number of the variations were also associated with coronary artery disease, type 2 diabetes, obesity, and high blood pressure.

The research also reveals that triglycerides - another type of blood lipid - play a larger role in heart disease risk than previously thought.

The results increase by more than a third the total number of genetic variants linked to blood lipids. All but one of the variants associated with blood lipids are near stretches of DNA that encode proteins.

Lead author Cristen Willer, Ph.D., assistant professor of Internal Medicine, Human Genetics and Computational Medicine and Bioinformatics at the U-M Medical School, said that these results give us 62 new clues about lipid biology, and more places to look than we had before.

A further analysis of the massive dataset, published as a letter with lead authors Sekar Kathiresan and Ron Do from Harvard University and the Broad Institute, suggests that triglyceride levels have more impact on cardiovascular disease risk than previously thought.

This analysis found that genetic variations that increase triglyceride or LDL-cholesterol levels are also associated with higher incidence of heart disease. But the analysis also casts further doubt on the role of high density lipoprotein, known commonly as HDL or "good cholesterol", in heart disease risk. In recent years, many drugs that modify HDL cholesterol have failed to show a benefit in preventing heart disease.

The findings have been published in the journal Nature Genetics.

--ANI (Posted on 07-10-2013)

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