Nav: Home

Targeting inflammation to better understand dangerous blood clots

May 28, 2019

It's the third deadliest cardiovascular diagnosis, but doctors are still often stumped to explain why 40% of patients experience unprovoked venous thromboembolism (VTE). And after a patient has dealt with these dangerous blood clots once, a second and subsequent events become much more likely.

New research from a team of University of Michigan scientists may help solve the mystery of how to detect and deal with higher-than-usual clot risk in patients' veins. The study, done in mice and published in the Journal of Clinical Investigation, focuses on clots' relationship to the body's defense and repair system, which causes inflammation.

"We don't yet understand the molecular triggers which drive the development of life-threatening clots in deep veins," said Yogen Kanthi, M.D., the study's senior author and a vascular cardiologist at U-M's Frankel Cardiovascular Center. "Our work aimed to identify and block a previously unrecognized pathway linking inflammation and thrombosis."

Kanthi, also an assistant professor of internal medicine at Michigan Medicine, says VTE is triggered by some combination of coagulation and inflammation. But current treatments come up short, he says, because they only focus on one side of the equation: anticoagulation. After VTE, patients are often prescribed blood thinners for life.

Kanthi's lab is instead investigating inflammation's role in the development of deep vein thrombosis. His team's new study found an enzyme called CD39 diffused circulating "danger" signals and inflammatory cytokines in blood during thrombosis.

FDA-approved drugs already exist for other conditions that are affected by the same pathway, and in particular, the paradigmatic inflammatory cytokine molecule called interleukin-1 beta. In fact, when the researchers inhibited interleukin-1 signals in their study, they reduced the number and size of venous blood clots the animals formed, Kanthi said.

"Here, we focused on potential therapeutics at the intersection of inflammation and thrombosis," Kanthi said. "We showed that blocking interleukin 1 beta, a ubiquitous inflammatory molecule, was a powerful means to stop clot formation."
-end-
Earlier this year, Kanthi and colleagues published a paper in Arteriosclerosis, Thrombosis, and Vascular Biology that identified CD39 as important to the venous thromboinflammatory response.

For updates on this and other research out of the Kanthi Lab, follow Kanthi on Twitter @YogenKanthi.

Additional authors, all from the University of Michigan, include co-first authors Vinita Yadav and Liguo Chi, Raymond Zhao, Benjamin Tourdot, Srilakshmi Yalavarthi, Benjamin N. Jacobs, Alison Banka, Hui Liao, Sharon Koonse, Anuli C. Anyanwu, Scott Visovatti, Michael Holinstat, J. Michelle Kahlenberg, Jason S. Knight and David J. Pinsky.

Michigan Medicine - University of Michigan

Related Inflammation Articles:

Why beta-blockers cause skin inflammation
Beta-blockers are often used to treat high blood pressure and other cardiovascular diseases.
How do ketogenic diets affect skin inflammation?
Not all fats are equal in how they affect our skin, according to a new study in the Journal of Investigative Dermatology, published by Elsevier.
The 'inflammation' of opioid use
New research correlates inflammation in the brain and gut to negative emotional state during opioid withdrawal.
Using a common anticonvulsant to counteract inflammation
The interaction between a chromosomal protein called HMGB1 and a cellular receptor called RAGE is known to trigger inflammation.
The inflammation connection
New biological findings point towards a new avenue for the development of anti-inflammatory drugs.
Stopping inflammation from becoming chronic
An international research team led by Friedrich Schiller University in Jena has developed a highly sensitive cell model to study the complex effects -- and side effects -- of anti-inflammatory drugs, with the ultimate aim of preventing chronic inflammation.
Microglia react distinctively during inflammation
Researchers from the Luxembourg Institute of Health (LIH) conducted a pioneering study to unravel the genetic programs triggered upon inflammation in microglia, specialized resident immune cells of the central nervous system.
To resolve inflammation, location matters
A single protein can both restrain the initiation of inflammation and help to actively resolve it, according to new research led by George Hajishengallis of the University of Pennsylvania and Triantafyllos Chavakis of Technical University of Dresden.
New inflammation inhibitor discovered
A multidisciplinary team of researchers led from Karolinska Institutet in Sweden have developed an anti-inflammatory drug molecule with a new mechanism of action.
Patchy distribution of joint inflammation resolved
Chronic inflammatory rheumatic diseases such as rheumatoid arthritis (RA) and spondylo-arthritis (SpA) are chronic disabling diseases that have a poor outcome on loco-motoric function, if left untreated.
More Inflammation News and Inflammation Current Events

Top Science Podcasts

We have hand picked the top science podcasts of 2019.
Now Playing: TED Radio Hour

In & Out Of Love
We think of love as a mysterious, unknowable force. Something that happens to us. But what if we could control it? This hour, TED speakers on whether we can decide to fall in — and out of — love. Guests include writer Mandy Len Catron, biological anthropologist Helen Fisher, musician Dessa, One Love CEO Katie Hood, and psychologist Guy Winch.
Now Playing: Science for the People

#542 Climate Doomsday
Have you heard? Climate change. We did it. And it's bad. It's going to be worse. We are already suffering the effects of it in many ways. How should we TALK about the dangers we are facing, though? Should we get people good and scared? Or give them hope? Or both? Host Bethany Brookshire talks with David Wallace-Wells and Sheril Kirschenbaum to find out. This episode is hosted by Bethany Brookshire, science writer from Science News. Related links: Why Climate Disasters Might Not Boost Public Engagement on Climate Change on The New York Times by Andrew Revkin The other kind...
Now Playing: Radiolab

An Announcement from Radiolab