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Sunday, November 17, 2024

Tulane researchers receive American Heart Association grant to study COVID’s vascular effects

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The American Heart Association has awarded Tulane University  researchers $940,000 to study how COVID-19 spurs vascular inflammation  that may increase risks for blood clots and lingering symptoms of long  COVID. 

The grant is one of 11 recently awarded by the American Heart  Association as part of a $10 million effort to study the cardiovascular  and cerebrovascular impacts of COVID-19 as the pandemic enters its third  year.

Tulane researchers will investigate the role that endothelial cells  play in the development of severe and long COVID-19. Endothelial cells  line blood vessel walls throughout the body and can malfunction  following SARS-CoV-2 infection. This dysfunction can cause  over-coagulation and blood clotting in major organs such as the heart  and lungs, as seen in the most severe COVID cases. It may also  contribute to complications associated with long COVID.

Dr. Xuebin Qin, professor of microbiology and immunology at the  Tulane National Primate Research Center, will lead a cross-disciplinary  team with the Tulane University School of Medicine to explore how the  dysfunction of endothelial cells contributes to severe and long COVID  outcomes.  

The team developed transgenic mouse models genetically engineered to  simulate COVID in the way that humans experience the most severe  outcomes of the disease, including the development of ARDS, or Acute  Respiratory Distress Syndrome. 

In the human population, those who experienced ARDS also had  endothelial cell injury, causing a weakening of the “tight junctions”  that normally serve to connect endothelial cells. If these junctions  weaken and leak, blood can escape and pool in the tissues of major  organs, causing abnormal clotting and tissue damage. 

It is the dysregulation of these tight junctions, they propose, that  contributes to severe and long COVID outcomes, particularly those  related to the vasculature of the heart and brain. 

“The health outcomes associated with COVID extend far beyond the  respiratory system,” Qin said. “By understanding how SARS-CoV-2  infection triggers endothelial cell dysfunction, we hope to open the  door to new therapies that prevent the cascade of effects that we see in  the most severe and lasting COVID cases.” 

Qin is the principal investigator; co-investigators include Dr. Jay  Kolls, John W Deming Endowed Chair in Internal Medicine; Dr. Patrice  Delafontaine, professor of medicine, pharmacology and physiology; Yusuke  Higashi, PhD, associate professor of medicine; Nicholas Maness, PhD,  associate professor of microbiology and immunology; and Stephen Braun,  PhD, assistant professor of pharmacology. 

Original source can be found here.

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