New York: Researchers have identified 36 new genes that plays a causal role in cardiac hypertrophy — abnormal thickening of the heart muscle — which can lead to heart failure.
“This is an exciting direction for personalised medicine, and also for identifying genes and therapeutic targets for complex diseases that involve many genes,” said co-author of the study Alain Karma, professor at the Northeastern University.
According to the Centres for Disease Control and Prevention, one in four deaths in the US each year are due to heart disease.
“The framework described in the paper can also be used to predict whether individuals suffering from a particular disease will respond to a given drug treatment,” said lead author Marc Santolini, a postdoctoral research associate at Centre for Complex Network Research.
For the study, published in the journal npj Systems Biology, the researchers took an entirely different approach — using the Hybrid Mouse Diversity Panel, a collection of 100 genetically different strains of mice that can be used to analyse the genetic and environmental factors underlying complex traits.
Within each strain, the mice are inbred, making them all identical twins on a genetic level.
Researchers took two mice from the same strain and gave one of them a stressor drug that induces heart failure. They then compared the stressed mouse’s gene expression with its non-stressed twin.
Since the mice have the same genome, they were able to pinpoint individual genes that changed expression as a direct result of the heart stressor.
Among the identified 36 such genes, many of these genes were previously unknown to be implicated in heart failure, the researcher said.
They mentioned that one of them is known as a transcription factor, meaning it controls the expression of many other genes.
They confirmed the gene’s role by using molecular biology techniques to silence it and observe the resulting changes of expression.
They found the transcription factor gene was directly connected to a whole network of proteins known to play a role in cardiac hypertrophy.