New genetic risk factor for heart disease identified

The mechanism by which a single gene influences a person's risk of cardiovascular disease has been described by US researchers.

The gene has far-reaching effects because it controls a network of other genes and cellular processes, playing an essential role in determining a person's genetic risk for heart attacks, aneurysms, and coronary artery disease.

Dr Clint Miller, from the University of Virginia, who led the study said: 'By gaining insight into the gene regulatory networks that underlie specific vascular disease pathways, we can develop more tailored interventions or risk metrics for patients.'

The study, published in the journal Circulation Research, was a collaboration between scientists from the University of Virginia, Harvard University and the New York Icahn School of Medicine.

The researchers used epigenetic profiling and analysis of human coronary artery tissue to understand how the gene FHL5 contributes to the development of multiple forms of cardiovascular disease.

The researchers found that when FHL5 was highly active, it caused an accumulation of high levels of calcium inside smooth muscle cells. Smooth muscle cells are an essential component of arteries while high calcium levels in cells can lead to arteriosclerosis and the build-up of plaques that can cause heart attacks and strokes.

'This is the first case where we found this factor to change functions of smooth muscle cells from the coronary artery,' said Dr Miller.

Furthermore, in the study, FHL5 contributed to reshaping of the coronary arteries over time as it regulates a network of other genes that have been associated with heart disease.

While many factors such as smoking, obesity, diabetes, and large consumption of red meat increase the risk for heart disease it has previously been challenging to isolate the effects of genetic components.

The researchers hope that because FHL5 strongly influences the development of arteriosclerosis, it could be a promising target for preventative drug treatments to reduce its activity. However, more research would be needed before such a treatment could be developed.

'Translating this knowledge to the clinic will require ongoing interdisciplinary collaborations, and we look forward to ultimately seeing the impact of these genetic studies,' said Dr Miller.