Endothelial cell calcium influx pathways

Endothelial cell calcium influx pathways represent the integrated network of ion channels and signaling proteins that facilitate the entry of Ca2+ into the vascular endothelium, a process essential for cardiovascular homeostasis [PMID: 23507082]. These pathways primarily include store-operated calcium entry (SOCE), mediated by the STIM1-Orai1 complex, and various transient receptor potential (TRP) channels such as TRPV4, TRPC1, and TRPC4 [PMID: 28213294, PMID: 31654649]. Calcium influx triggers the production of vasodilators like nitric oxide (NO) and prostacyclin, thereby regulating vascular tone and blood pressure [PMID: 22539641]. Additionally, these pathways are critical for maintaining the endothelial barrier and promoting angiogenesis [PMID: 25633151]. Dysregulation is associated with hypertension, atherosclerosis, and inflammatory lung injury [PMID: 28213294]. While specific channels within these pathways are targeted by experimental compounds like GSK2193874 (TRPV4 antagonist), the term refers to a broad physiological process rather than a single molecular target [PMID: 31654649]. Therapeutic strategies often focus on modulating specific channel activity to restore endothelial function or prevent pathological permeability. However, the ubiquity of calcium signaling poses significant challenges for achieving tissue-specific effects without systemic toxicity.

Other names

Endothelial calcium signalingStore-operated calcium entry (SOCE)Receptor-operated calcium entry (ROCE)Endothelial TRP channel signaling

Modulation of intracellular calcium levels through the inhibition or activation of specific calcium-permeable channels such as TRPV4 or Orai1 [PMID: 28213294].