New research has pinpointed two genes that can trigger “good” or “bad” cardiovascular health. The genes were identified as ANGPTL4 and SVEP1.
The genetic information has come from a review of DNA data from 190,000 people living in the U.S. The analysis revealed 220,000 genetic variants that altered proteins. These were examined to see which types influenced heart disease risk. It is known that coding errors with proteins can be associated with heart attacks.
The data showed an error with the ANGPTL4 gene could lead to a reduction in heart attacks, whereas an error with the SVEP1 gene increased the chance of having a heart attack by around 14 percent. The reason is due to an association with SVEP1 and high blood pressure.
The ANGPTL4 gene, as noted in the research brief, plays a role in the body’s processing of triglycerides. Triglycerides are fats found in the blood (high levels act as a biological marker for suspect heart attacks). This inferred a fault with the ANGPTL4 gene could lead to a greater build-up of the potentially harmful fats.
It is hoped the new information could lead to the development of preventative drugs to promote heart health. These would be drugs designed to work on the major pathway regulating triglycerides. The drugs would act to slowdown the build-up of plaque within the coronary arteries, which should confer protection against heart attacks.
Lead researcher Dr. Nathan O. Stitziel told Bioscience Technology: “The gene’s (ANGPTL4) association with lower triglycerides has been known for a while. But for a long time it was not clear that high triglycerides were a cause of coronary disease rather than a marker of it. Now we know that errors in ANGPTL4 associate with both reduced triglycerides and lower risk of coronary disease. This is another piece of the puzzle that points to a causal role for triglycerides in coronary disease.”
The study was carried out at Washington University School of Medicine in St. Louis together with the Broad Institute at Massachusetts Institute of Technology and Harvard University. The findings are published in the New England Journal of Medicine. The paper is titled “Coding Variation in ANGPTL4, LPL, and SVEP1 and the Risk of Coronary Disease.”
