American Heart Association award supports advanced research into pulmonary fibrosis
Samar Antar, a postdoctoral associate with the Fralin Biomedical Research Institute at VTC, will use the Career Development Award to identify new therapeutic targets for the progressive, irreversible lung disease.
Samar Antar has received a Career Development Award from the American Heart Association that could help her uncover new therapeutic strategies for pulmonary fibrosis, a progressive and fatal lung disease with limited treatment options.
The award supports Antar’s work in understanding how the protein connexin 43 (Cx43), which enables communication between cells, drives disease progression. By investigating how this pathway regulates lung fibroblasts, cells that rebuild connective tissue, she anticipates that her work could lead to therapies that not only slow disease progression, but actively reverse lung damage.
Idiopathic pulmonary fibrosis arises from unknown causes and is characterized by excessive scarring of lung tissue, leading to declining lung function and, ultimately, respiratory failure. Co-occurring arrhythmias, coronary artery disease, and heart failure are common. Roughly 100,000 people in the United States are living with the disease, according to the Pulmonary Fibrosis Foundation.
“Despite advances in treatment, there is currently no cure,” said Antar, a postdoctoral associate working in the lab of Yassine Sassi, assistant professor with Virginia Tech’s Fralin Biomedical Research Institute at VTC. The Sassi lab conducts research into new therapies for heart and lung diseases.
Antar’s research focuses on gap junction intercellular communication, which allows cells to exchange signals and coordinate behavior. She will examine how Cx43, the most widely expressed gap junction protein, helps regulate cell growth, differentiation, and inflammation in scar-forming cells.
Antar’s preliminary research has identified that Cx43 expression is elevated in lung fibroblasts in tissue samples from patients with the disease and in animal models.
“My overall goal is to determine whether inhibiting Cx43 can reverse pulmonary fibrosis,” Antar said. In preclinical studies, inhibiting Cx43 reduced fibroblast activation and improved lung function, pointing to its potential as a therapeutic target.
Antar received a bachelor’s degree in pharmaceutical sciences from Sinai University and master’s and doctoral degrees from Zagazig University and Suez Canal University, all in Egypt. After completing her master’s degree, she studied the development of fibrosis during cancer treatment.
The American Heart Association Career Development Award is designed to support promising early-career investigators as they establish independent research programs. The funding will enable Antar to expand her research portfolio while receiving mentorship and training.
