Local vascular permeability enhancement via ultrasound-mediated acoustic cavitation (None)

This "target" refers to the temporary, local increase in vascular permeability initiated by focused or pulsed ultrasound energy—often in combination with circulating microbubbles—which mechanically disrupts endothelial cell junctions (via acoustic cavitation and radiation force) at a targeted site. The resulting reversible permeabilization of vessels is used to facilitate the delivery of therapeutics, particularly large molecules or nanoparticles that would not ordinarily cross vascular barriers such as the blood-brain barrier. The approach does not engage a single molecular target, but rather exploits physical effects and endothelial cell responses (including nitric oxide signaling, cytoskeletal rearrangement, and caveolin-1 mediated transport). The effect is transient and spatially controllable, but requires cautious dosing to avoid vascular injury. Its main applications are in research and emerging clinical settings to improve drug delivery for cancer and CNS diseases. Key point: This entry refers to a technique/physical process, not a discrete molecular therapeutic target like a receptor or enzyme. For structured biomedical data models, it should not be classified as a molecular target.

Other names

Ultrasound-induced vascular permeabilityFocused ultrasound-mediated vascular permeabilityBlood-brain barrier opening via focused ultrasoundAcoustic cavitation-mediated permeability

Transient disruption of endothelial tight junctions by mechanical and shear forces; Enhanced caveolae-mediated transcellular transport via upregulation of caveolin-1; Pore formation in endothelial membranes via inertial cavitation