Jason Dyck, professor in the Division of Pediatric Cardiology and director of the Faculty of Medicine & Dentistry's Cardiovascular Research Centre, is receiving $716,000 over five years from a 2019 CIHR project grant.
In this Q & A, Jason Dyck explains how funding from the Canadian Institutes of Health Research (CHIR) will help address adipose tissue inflammation and its role in heart failure. Adipose tissue is one way the body stores fat. Heart failure affects between 1.5 and two per cent of Canadians and is the most common cause of hospitalization. Clinical heart failure happens when the heart is prevented from pumping enough blood to the rest of the body.
What is the research focused on?
My lab has been investigating the different mechanisms that contribute to heart failure, such as the contribution of other organs to poor health outcomes in heart failure patients. When you have heart failure, changes occur in the heart but also in the fat cells - the adipose tissue. Those fat cells sense heart failure. In response, they get modified or change their function and secrete specific chemicals or proteins that will go into the bloodstream and signal back to the heart. The heart senses these signals and responds negatively such that heart function is further impaired. So there's this link between the heart and adipose tissue. We can target the adipose tissue with a new drug that has been synthesized and only works in fats cells. By just targeting fat cells, we are able to prevent worsening heart function and heart failure. To me, it's really exciting when you can impact heart function by targeting fat cells.
What inspired this research?
There's a paper that came out that showed this connection between the heart and signals to the adipose tissue. We thought we should investigate. It was published in 2013 and there were no tools to investigate it further. Since then, we developed a mouse knockout of this gene we wanted to target. There weren't any drugs available so we wanted to knock the gene out only in the adipose tissue. While we were working on that, collaborators identified a drug that did the exact same thing and targeted primarily adipose tissue. We used that drug and found almost identical results.
What will the funding allow you to do?
We know that there's a signal for adipose tissue governed by this one particular protein that we've targeted genetically. Now we need to know what it is signalling. What is it releasing into the blood? The idea would be instead of targeting adipose tissue, we could identify something in the heart that's being changed by the adipose tissue. We can develop new drugs that can be used specifically on the heart.
What kind of impact will the research will have on patients?
Finding a new treatment strategy for approved or additional treatment for heart failure is extremely important. Once you have heart failure, the therapies aren't great. Mortality is 30 to 50 per cent after the first two years and heart patients are one of the most expensive to treat.
How far along is your research?
Fortunately we have been able to build some of the tools like the knockout mouse and we have the drugs in-house. We also have the preliminary data that shows this is a viable approach. The next step is to be able to roll all of this out and get a clear understanding of how important this is. This could be a blockbuster in heart failure therapy. It could also completely fail. Unless we do this and test it, we won't know and we could be missing a huge opportunity in heart failure therapy. This is why we do the research. We drive it as far as we can.
What is the research focused on?
My lab has been investigating the different mechanisms that contribute to heart failure, such as the contribution of other organs to poor health outcomes in heart failure patients. When you have heart failure, changes occur in the heart but also in the fat cells - the adipose tissue. Those fat cells sense heart failure. In response, they get modified or change their function and secrete specific chemicals or proteins that will go into the bloodstream and signal back to the heart. The heart senses these signals and responds negatively such that heart function is further impaired. So there's this link between the heart and adipose tissue. We can target the adipose tissue with a new drug that has been synthesized and only works in fats cells. By just targeting fat cells, we are able to prevent worsening heart function and heart failure. To me, it's really exciting when you can impact heart function by targeting fat cells.
What inspired this research?
There's a paper that came out that showed this connection between the heart and signals to the adipose tissue. We thought we should investigate. It was published in 2013 and there were no tools to investigate it further. Since then, we developed a mouse knockout of this gene we wanted to target. There weren't any drugs available so we wanted to knock the gene out only in the adipose tissue. While we were working on that, collaborators identified a drug that did the exact same thing and targeted primarily adipose tissue. We used that drug and found almost identical results.
What will the funding allow you to do?
We know that there's a signal for adipose tissue governed by this one particular protein that we've targeted genetically. Now we need to know what it is signalling. What is it releasing into the blood? The idea would be instead of targeting adipose tissue, we could identify something in the heart that's being changed by the adipose tissue. We can develop new drugs that can be used specifically on the heart.
What kind of impact will the research will have on patients?
Finding a new treatment strategy for approved or additional treatment for heart failure is extremely important. Once you have heart failure, the therapies aren't great. Mortality is 30 to 50 per cent after the first two years and heart patients are one of the most expensive to treat.
How far along is your research?
Fortunately we have been able to build some of the tools like the knockout mouse and we have the drugs in-house. We also have the preliminary data that shows this is a viable approach. The next step is to be able to roll all of this out and get a clear understanding of how important this is. This could be a blockbuster in heart failure therapy. It could also completely fail. Unless we do this and test it, we won't know and we could be missing a huge opportunity in heart failure therapy. This is why we do the research. We drive it as far as we can.