Graduate student pursues potential therapy for deadly lung disease
An American Heart Association fellowship recognizes Dilruba Yeasmen’s research into an essential signal control that has the potential to inhibit lung scarring.
With no cure in sight, idiopathic pulmonary fibrosis kills roughly 22,600 Americans each year. Virginia Tech doctoral student Dilruba Yeasmen is working to halt the deadly lung disease.
A student in the Translational Biology, Medicine, and Health Graduate Program, Yeasmen has been awarded a predoctoral fellowship from the American Heart Association. The award will support her research on idiopathic pulmonary fibrosis (IPF), a chronic and fatal lung disease with limited treatment options.
IPF primarily affects older adults and is characterized by progressive scarring of lung tissue that impairs breathing. Despite advances in diagnosis, there is no cure, and half of patients typically survive for less than four years after diagnosis.
“My research focuses on a protein that acts like a brake on the signals that cause lung scarring. If we can restore that brake, we may be able to stop the disease in its tracks — and for patients who currently have so few options, that would be enormously meaningful,” Yeasmen said.
Yeasmen’s work focuses on the role of a protein known as SARA, short for Smad anchor for receptor activation. The protein helps regulate Transforming Growth Factor-beta (TGF-beta) signaling, which drives fibrosis. She’s conducting her research in the lab of Yassine Sassi, associate professor at Virginia Tech’s Fralin Biomedical Research Institute at VTC.
Yeasmen’s preliminary findings show that SARA levels are significantly reduced in fibrotic lungs and in lung fibroblasts exposed to profibrotic signals such as TGF-beta.
Her studies suggest that restoring SARA expression may counteract the processes that lead to lung scarring. In laboratory experiments, increasing SARA levels reduced fibroblast proliferation, migration, and differentiation, which drive fibrosis. In animal models, restoring SARA levels prevented the development of pulmonary fibrosis and improved lung function.
Using advanced molecular and imaging approaches, the fellowship will help Yeasmen investigate how SARA modulates TGF-beta signaling and whether targeted delivery of SARA to lung fibroblasts can reduce fibrosis and restore lung function.
“Dilruba has done remarkable work uncovering a role for SARA that nobody in the field had explored before. What excites me most is that this isn't just a basic science finding. It points toward a concrete therapeutic strategy. By delivering SARA specifically to the lung, we're aiming to interrupt fibrosis at its source, and this fellowship will allow her to take that work to the next level,” said Sassi, who also holds an appointment in biomedical sciences and pathobiology at the Virginia-Maryland College of Veterinary Medicine.
By uncovering how SARA regulates fibrotic signaling and testing strategies to restore its function, Yeasmen’s work aims to identify a novel therapeutic approach for IPF.
If successful, the research could lay the groundwork for treatments that directly target the underlying mechanisms of fibrosis and offer hope for patients with this life-threatening disease.
The American Heart Association Predoctoral Fellowship supports outstanding graduate students conducting research in cardiovascular, cerebrovascular, and related fields, with the goal of developing the next generation of scientific leaders.
