Editor’s note: This is one in a series of Cardiovascular Genome-Phenome Study Discovery grants to speed personalized treatments and prevention for heart disease.

Piece by piece, researchers are working on different parts of the puzzle to control and cure heart disease. At Mount Sinai, Ron Do, Ph.D., is working on the genetic puzzle piece.

Do and his co-investigators hope to identify how a person’s genes and environment interact to construct someone’s phenotype — characteristics you can see, such as eye color and height, and those you can’t, such as behavior and metabolism — and which of those traits contribute to heart disease. Right now those things are a mystery to researchers.

“Coronary heart disease is one of the leading causes of death and infirmity worldwide. After age 40, one in two men and one in three women will develop a coronary event in their lifetime,” said Do, an assistant professor at the Charles R. Bronfman Institute for Personalized Medicine in the department of genetics and genomic sciences at Mount Sinai’s Icahn School of Medicine.

Last November, Do was among 10 researchers each awarded $160,000 to study ways to individualize the treatment and prevention of heart disease. These grants, which are funded by AstraZeneca, probe three areas: heart failure, “good” HDL cholesterol and predicting cardiovascular disease.

“I look at this research of studying the genetics of coronary heart disease as a series of puzzles where I am constantly thinking about methods and working out solutions,” Do said. “I am excited about the implications of our research, which include identifying novel biological pathways and mechanisms for coronary heart disease.”

His team will examine known genes involved in heart disease in people already with the condition, and see if those with DNA that is strung together differently have distinct cardiovascular risk factors.

Do also wants to know which risk factors to target with new drugs that aim to lower heart disease risk. Along the way, his team will search for the gene culprits that affect those risk factors. It’s an approach that was successfully used to confirm that higher levels of “bad” LDL cholesterol increase the risk for heart disease.

In his current work, Do hopes to identify additional risk factors that cause disease.

“Current cholesterol-lowering agents such as statin therapy are not effective in a fraction of individuals, while some experience adverse side effects that prevent them from taking the drugs,” he said. “So there is a need to develop novel therapeutics for heart disease.”

Read other stories in this series.