TRP channels in uterine pathophysiology- A short review

Abstract

Calcium ions are major upstream signalling molecules to initiate myogenic contraction. TRP (Transient receptor potential) proteins belong to cation channel protein family and are localized in the cell membrane. The most perform of TRPC is to control the inflow of Ca2+ / Na+ batting on PKC pathway activation evoked by G-protein-coupled receptors (GPCR). TRPV6, is mostly expressed in pregnant uterus in human, mouse, rat and pig. TRPV6 and TRPC1 are related to embryo implantation. Upregulated TRPC3 urged to play an important role in LPS-induced preterm labor. TRPC1 and TRPM7 are rumoured to related to abnormal uterine fibroid contraction. TRPV4 channels are present within the pregnant and nonpregnant mouse uteri, and their activation by prostaglandin increases myometrial contractility. TRPA1 over activity could also be related to pre-eclampsia and connected cardiovascular diseases. So with growing evidences of upregulation of varied TRP proteins in several pathological conditions of the uterus in human and experimental animals signifies TRP proteins rising as a new therapeutic target in uterine pathophysiology.