Sydney: A gene network behind the hardening of coronary arteries and heart disease has been identified by a team of scientists from Australia, Europe and Britain.
Researchers from Australia`s Walter and Eliza Hall Institute, Finland`s National Institute for Health and Welfare, the University of Helsinki and Leiden University Medical Centre in The Netherlands were involved in the study.
Concentrations of cholesterols (waxy substance found in the cell membranes) that severely restrict blood flow in the heart muscle, causing chest pains, are an important predictor of coronary artery disease, the most common form of heart disease.
Coronary artery disease refers to "hardening of the arteries," or atherosclerosis, a cycle where cholesterol builds up on the walls of arteries and the body`s resultant immune response leads to more build-up, according to Walter and Eliza statement.
To investigate how cholesterols in the blood stream activate circulating immune cells, the researchers looked at samples from more than 500 volunteers to construct biological networks of genes that move in concert.
Circulating immune cells are integrated system of organs, tissues, cells, and cell products such as antibodies that neutralise potentially harmful organisms or substances.
The volunteers were participants in Finland`s Dietary, Lifestyle and Genetic determinants of Obesity and Metabolic syndrome (DILGOM) study.
Michael Inouye, postdoctoral fellow at the Walter and Eliza Hall Institute, who conducted the research, said the study identified a network of genes whose activity was tied to the level of cholesterol in the blood, reports the journal Public Library of Sciences-Genetics.
"These genes look like an inflammatory network and appear reactive to high-density lipoprotein,(which enable fats to be carried in the blood stream), triglycerides, (fatty deposits in coronary arteries and liver)... all of which are predictors of downstream cardiovascular disease," he said.
"We are just beginning to understand biological networks and how they relate to disease," Inouye said.