Newswise — So many of us have lost loved ones to heart disease and stroke. According to the American Heart Association, someone dies from a heart attack every minute in the United States, and stroke kills an American about every four minutes.
Ulhas Naik, director of the Delaware Cardiovascular Research Center based at the University of Delaware, is now on the trail of what may be a key accomplice to these leading killers of humankind.
Naik’s focus is ASK1 (apoptosis signal-regulating kinase 1), an enzyme found in blood platelets, the tiny cells that rush to the scene to form a clot where a blood vessel is injured or a plaque inside an artery has ruptured. Naik has received a four-year, $1.53 million grant from the National Heart, Lung, and Blood Institute of the National Institutes of Health to support the research project.
“What’s so interesting about ASK1 is that it is activated only by stress,” Naik says. “When under stress, ASK1 signals other proteins critical to cell survival to stimulate the platelets to get to work.”
After they are made in your body’s bone marrow, platelets circulate in the blood stream, where they live for eight to 10 days. When an injury occurs, these tiny disks start sticking to the wound site and put out tentacles that help them clump together to plug the leak. While clot formation is critical for getting a cut finger to stop bleeding, it can be deadly inside a blood vessel when it prevents blood flow, causing a heart attack or stroke.
“In our laboratory studies, we’ve found for the first time that lots of ASK1 protein is expressed in platelets and is rapidly activated when a blood vessel is injured or is under stress from free radicals or from a lack of oxygen, for example. We believe this is an important stress-response signaling pathway,” Naik notes.
In his laboratories in UD’s Department of Biological Sciences and at the Delaware Biotechnology Institute, Naik and his research team are working to synthesize a new compound to block the ASK1 function and thus inhibit the platelets’ clotting function. Key to the project’s success will be formulating the inhibitor in such a way that it will stop excess clot, or thrombus, formation without affecting the beneficial process of wound healing.
“We’re taking a step forward in developing a new thrombotic drug,” Naik says. “My goal is not to make money, but to find something that will help control devastating diseases like stroke and atherosclerosis.”
Naik knows the heartbreak of these killers firsthand. Three of his brothers have died from heart attacks.
About project support
The research reported in this news story is supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health (NIH) under NIH grant award number RO1HL11318801A1.
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