Inhibiting the interaction between thrombospondin-1 and CD47 protects non-target tissues from radiation damage, allowing higher doses to enhance tumor ablation.
Applying controlled extensional and shear strains to prefibrillar solutions overcomes poor collagen organization in seeded cell methods.
Inhibiting Cthrc1 expression improves cardiac perfusion by promoting outward vascular remodeling without increasing myocardial oxygen demand.
Isolated anti-integrin α9 inhibitors block integrin α9β1 activity to limit brain damage following reperfusion after ischemic stroke.
Biotinylated antibodies recruit reparative cells to damaged cartilage via avidin bridges, preventing systemic side effects from non-specific drug delivery.