Anti-fibrotic drug could be repurposed to control cell communication

Scientists at the University of Surrey have discovered that an experimental antifibrotic compound called SD-208 can dramatically alter how cells release the microscopic packages they use to communicate with each other. The compound reduces scar tissue in organs but also substantially decreases the release of extracellular vesicles, tiny carriers of proteins and other biological signals.

Instead of being transported to the cell surface and released, the vesicle-containing compartments are redirected toward lysosomes, the cell's recycling and disposal system. This unexpected effect was observed in cardiac cells taken from patients with hypertrophic cardiomyopathy, a condition characterized by abnormal thickening of the heart muscle.

Researchers found that SD-208 not only stopped the vesicles from being made but changed their destination inside the cell, directing them towards lysosomes. While SD-208 exhibited the same effect in several different types of cells, it did not reproduce this effect with other compounds acting on the same primary target. This suggests a mechanism distinct from its antifibrotic activity.

The researchers noted that while SD-208 redirected vesicle-containing compartments toward lysosomes, the therapeutic potential of this finding remains unproven, as it was observed only in laboratory-grown cells.