Cardiovascular disease is the number one cause of death on the planet. It has many causes: from smoking, diabetes, high blood pressure, to air pollution, and rare conditions such as cardiac amyloidosis. Of all the tissues in the heart, cardiomyocytes are one the most important muscles groups to keep the heart functioning.

As the chief cell type of the heart, cardiomyocytes are responsible for generating contractile force, keeping blood pumping throughout the body. When these muscle cells die, heart failure occurs with devastating results.

But GlycoNet Investigators Dr. Mona Nemer from the University of Ottawa and Dr. Yvan Guindon from IRCM now have discovered molecules that could potentially protect cardiomyocytes from death. 

“If we treat cardiac cells with these molecules, we can prevent the cardiac cells from dying in response to anti-cancer treatment. This means we can preserve cardiac function and prevent heart failure,” says Nemer. 

While many things can lead to heart failure, including conditions such as hypertension, hardening of arteries, or complications from diabetes, the researchers focus on heart failure caused by chemotherapy.

“Some very effective anti-cancer drugs cannot be used at their optimal dose or with many people because it’s known they would lead to heart failure,” says Nemer. “Initially we set out to develop a way to protect the heart against heart failure that is induced by cancer treatment. We’re hoping that any developments will also be expanded to other types of heart failure.”

The team has already demonstrated the success of their lead molecule both in culture and in animal testing, and is hoping to continue to advance towards treatment of a disease that has unmet clinical needs. Heart failure is the number one reason for hospitalization in people over 65.

“It’s a very serious condition,” says Nemer. “Right now, there are no therapies available to stop, slow down, or cure heart failure. As a result, it’s a diagnosis that can be worse than some cancers. Fifty per cent of the individuals diagnosed with heart failure will die within five years.”

Whether the drug could also reverse heart failure once it has progressed will determine the breadth of application of the drug, and it’s something the team is still investigating.

“The results are very encouraging, showing that it can prevent the onset of heart failure in conditions where the heart has already started to go down that path,” says Nemer. “Some of the experiments we’d like to do moving forward are to see the extent to which the drug can be effective – can it be given at mid-course heart failure, at end-stage? Are we able to stabilize once the disease has set in and at what stage?”

The group will also be doing more extensive pre-clinical studies, with the hopes of eventually moving to clinical studies. Nemer credits their success so far to fundamental studies in carbohydrate chemistry and in the effects of anti-cancer drugs, which were applied together thanks to the collaboration enabled by GlycoNet.

“A project like this cannot be carried out except with a multidisciplinary team because it’s an iterative process,” she says. “That’s the goal of a network like GlycoNet – to take basic discoveries and enable their translation into innovations that can be of socioeconomic benefit.”