In a new study, researchers have found a potential drug to treat heart attacks and to prevent heart failure.
They have discovered what they believe is a novel drug target controlling the body’s repair responses after a heart attack.
The research was conducted by a team from the University of Guelph.
A leading cause of death worldwide, heart attacks trigger inflammatory responses that cause a scar to form in the heart. Over time, that damage eventually leads to incurable heart failure.
The circadian “clock” is found in virtually all cells of the body. It consists of genes and proteins that interact during the 24-hour day and night cycles to regulate key functions such as heart rate and blood pressure.
In the heart, that clock mechanism controls healthy cardiovascular physiology as well as how the heart responds to damage and undergoes repair.
In the study, the researchers used a drug called SR9009, which targets a key component of the cellular clock mechanism.
The medication disrupts the expression of genes that trigger adverse immune responses after a heart attack.
The team found administered within hours of an attack, the potential drug would prevent scarring.
It would also eliminate the need for patients to take possibly debilitating heart medication for the rest of their lives.
This is the first time scientists show that giving a treatment after a heart attack along with conventional therapy such as reperfusion could lead to less inflammation and better cardiac repair.
The team says the research is really exciting because it opens the door to use circadian medicine therapies to heal heart attacks after they occur and to prevent the subsequent development of heart failure.
If there is no scar, then there will be no heart damage and no heart failure. People can survive heart attacks because the heart won’t even be damaged.
The discovery might ultimately help in other heart therapies involving early adverse inflammatory responses such as organ transplant or valve replacement.
One author of the study is Prof. Tami Martino, Department of Biomedical Sciences.
The study is published in Nature Communications Biology.
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