IndraLab

"The transient receptor potential cation subfamily V member 1 (TRPV1) and member kcnk2 (TRPV2) channels are also reported to allow the passage of Ca current."

"Cultured human TM cells are highly mechanosensitive, responding to physiological (5–15 mm Hg) pressure steps with Na , K and Ca currents mediated by Piezo1, TRPV4 and TREK-1 channels (18–21)."

"Therefore, the differential expression of TREK-1 in different regions after infarction makes different regions differently sensitive to mechanical stretch, which may trigger different electrophysiological activities of ventricular myocytes and cause ventricular arrhythmias, such as ventricular fibrillation.In the permanent coronary artery ligation model, TREK-1 knockout mice showed longer QT interval, longer action potential duration, increased calcium consumption, larger infarct size, and more severe systolic dysfunction compared with wild type mice, which confirmed the protective role of TREK-1 in MIRI (Kamatham et al., 2019)."

"Another study has shown that NO production in endothelial cells requires TREK1 activity (16), in related studies TREK1 was thought to induce calcium flux and increase NO synthesis in endothelial cells (43–45)."

"Future studies will be focused on the complete molecular mechanism underlying Ca 2+ influx mediated by the basal TREK1 channel activity in HSCs.To elucidate the pathophysiological role of TREK1 channe[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"The up-regulated expression of KCNK1/KCNK2 channels has been suggested to shift the resting membrane potential in a hyperpolarizing direction, enhance Ca influx, and facilitate Ca -dependent signaling, including JNK (5)."

"TREK1 can also act as a gatekeeper for Ca homeostasis; for instance, Yarishkin et al. demonstrated that pharmacological activation of TREK1 using ML-402 initiated increased intracellular Ca [26]."

"Furthermore, TREK1 can facilitate the TRP channel-dependent Ca influx, and TREK1-dependent hyperpolarisations can stimulate Ca entry via tonically activated TRP-like channels [26,27,28]."

"Thus, in corticotropes, CRH causes the closure of background TREK-1 channels via a cAMP/PKA pathway and the resultant depolarization activates extracellular Ca 2+ entry via VGCC (summarized in Fig. 2 [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"We hypothesize that TREK-1 depolarization is not enough to induce a robust calcium entry."

"This in turn leads to the phosphorylation of TRPV1, other TRP ion channels, or TREK-1 channels, which then potentiates calcium influx during stimulation."