Researchers have identified a potential cellular and molecular driver of cardiac allograft vasculopathy, a chronic form of heart transplant rejection, according to a study published May 18 in Nature Cardiovascular Research.
Cross-collaborative teams from Stanford (Calif.) University, Washington University in St. Louis and Aurora-based University of Colorado analyzed coronary arteries from explanted hearts to establish a genetic and cellular signature of cardiac allograft vasculopathy.
“The analysis revealed that [cardiac allograft vasculopathy] is driven by close interactions between immune cells and stromal cells within the neointima, the abnormal new inner layer of the vessel wall that narrows the artery,” according to a June 10 news release from Palo Alto, Calif.-based Stanford Medicine.
Researchers were able to decrease the incidence and severity of cardiac allograft vasculopathy in mouse models by blocking specific cell signaling with ruxolitinib, pointing to a potential therapeutic target, the release said.
Read the full study here.
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