FIGURE 2.

Potential treatments of TRPV3 mutation-related OS. The activation of TRPV3 channels leads to Ca²⁺ influx, which causes a surge in intracellular Ca²⁺ signaling, promoting the release of TGF-α. TGF-α and EGF then activate their receptor EGFR, activating the EGFR/PI3K/AKT/mTOR cascade. TRPV3 antagonists (Dyclonine, Trpvicin, FTP-THQ, osthole, α-mangostin, forsythoside B, IAA, and IAB) inhibit the TRPV3 channel. Erlotinib and Sirolimus inhibit EGFR and mTOR respectively (PI3K: phosphatidylinositol-3-kinase; AKT: protein kinase B, PKB).