Schistosome voltage-gated calcium channel (Cav channel)

Schistosome voltage-gated calcium channels (Cav) are essential transmembrane protein complexes found in parasitic flatworms of the genus Schistosoma, the causative agents of schistosomiasis [1]. These channels are composed of a pore-forming α1 subunit and auxiliary subunits, most notably the β subunit (SmCavβ), which are critical for regulating calcium homeostasis and neuromuscular signaling within the parasite [2]. For decades, these channels have been recognized as the primary molecular target of praziquantel (PZQ), the standard treatment for schistosomiasis [3]. PZQ binding to the channel complex—specifically involving the variant β subunits unique to schistosomes—induces a rapid and sustained influx of calcium ions, leading to immediate spastic paralysis and severe damage to the parasite's protective tegument [4]. This tegumental disruption exposes parasite antigens to the host's immune system, facilitating the clearance of the worms [5]. While recent research has also identified specific transient receptor potential (TRP) channels as targets for PZQ, the voltage-gated calcium channels remain a central component of the parasite's physiological response to the drug and a key area for studying anthelmintic resistance [6].

Other names

Schistosome Ca2+ channelSchistosoma mansoni voltage-gated calcium channelSmCavVoltage-gated calcium channel beta subunitSmCavβ

Praziquantel acts as an allosteric modulator of the schistosome voltage-gated calcium channel complex, specifically interacting with or requiring the presence of the beta subunit to trigger a rapid and massive influx of calcium ions into the parasite.