Inhibition of Fgr Reduces Radiation-Induced Profibrotic Markers
Radiation-induced pulmonary fibrosis (RIPF) is a common, but severe, complication of sustained radiation therapy for clinical radiotherapy for lung cancer patients. RIPF can also occur in survivors of acute radiation syndrome as a delayed effect. Senescent cells have been implicated in both RIPF and idiopathic pulmonary fibrosis, but the molecular mechanism by which radiation-induced senescence (RIS) causes fibrosis is unknown, making the identification and targeted removal of senescent cells difficult.
Description
Using RNA-sequence analysis with a pure population of sorted radiation-induced senescent cells, University of Pittsburgh researchers found that Fgr mRNA is upregulated by more than 70-fold exclusively in senescent cells. Previous research does not implicate Fgr in RIS-induced lung fibrosis. Pharmacologic inhibition of Fgr in senescent cells reduced profibrotic gene expression in targeted cells, heralding the potential to prevent fibrosis from developing in individuals who have sustained radiation damage.Applications
• Preventing and treating RIPF in lung cancer patients receiving radiation therapy• Mitigating development of lung damage as a new radiation countermeasure