Endothelial cell calcium entry

Endothelial cell calcium (Ca2+) entry is a fundamental physiological process that regulates vascular tone, permeability, and angiogenesis (PubMed: 23507713). It is mediated by a variety of ion channels, including store-operated calcium entry (SOCE) channels such as Orai1 and STIM1, and transient receptor potential (TRP) channels, most notably TRPV4, TRPC1, and TRPC6 (PubMed: 25103161). In response to chemical stimuli like acetylcholine or mechanical forces like shear stress, these channels allow extracellular Ca2+ to enter the cytoplasm, triggering the production of vasodilators such as nitric oxide (NO) and prostacyclin (PubMed: 28807935). Dysregulation of this process is linked to cardiovascular diseases such as hypertension, pulmonary edema, and atherosclerosis, as well as pathological angiogenesis in cancer (PubMed: 22539488). Pharmacological targeting of specific channels involved in endothelial Ca2+ entry, such as the use of TRPV4 antagonists like GSK2798745, is an active area of research for treating vascular dysfunction and pulmonary congestion (PubMed: 22915715). However, achieving selectivity remains a challenge due to the ubiquitous nature of calcium signaling across different cell types.

Other names

Endothelial Ca2+ influxEndothelial calcium signalingStore-operated calcium entry (SOCE)Agonist-induced calcium entry

Modulation of calcium-permeable ion channels (e.g., TRPV4, Orai1, TRPC) to regulate intracellular calcium concentrations and downstream signaling pathways in the vascular endothelium.