The role of Ca(2+) in ultrasound-elicited bioeffects: progress, perspectives and prospects.

Intracellular calcium (Ca(2+)) transients have been observed in association with exposure to therapeutic ultrasound and correlated to both early- and late-onset bioeffects. For example, it has been suggested that early 'ultra-short' Ca(2+) transients recorded during sonoporation can mediate Ca(2+)-dependent exocytosis and endocytosis processes as complementary mechanisms for membrane self-sealing. Moreover, apoptosis induction has been reported to occur through a partial mediation of a Ca(2+)-dependent pathway. In this review, we attempt to assemble the salient facts into a cogent whole, with special attention given to the relationships arising through altered Ca(2+) levels, which underscore its crucial role during ultrasonic interactions with biological systems and its consequent implications in the context of therapeutics.