Massachusetts General Hospital researchers developed nanoparticles that target myofibroblasts in fibrotic lung tissue, using a peptide recognized by the angiotensin II type 2 receptor. Inhibiting the Rho/MRTF/SRF pathway was therapeutic in a mouse model of pulmonary fibrosis, with minimal off-target toxicity.
Rachel S. Knipe, MD, Benjamin D. Medoff, MD, and colleagues have shown in an animal model that an endothelial cell surface receptor, S1PR1, modulates the fibrotic response to lung injury. Agonism of its expression or function may be a novel and effective antifibrotic approach.
Within the next year, physicians can expect to see increased numbers of patients with fibrotic lung disease that has developed as a complication of acute respiratory distress syndrome related to COVID-19.