A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing
organ that regulates cardiovascular homeostasis. Disruption of endothelial integrity, as a result of either angioplasty or
stent deployment, may produce a late in-stent restenosis and limit the beneficial outcome of reconstructive vascular
surgery. Restoration of endothelial lining requires spreading, migration and proliferation of ECs nearby the lesion site.
Intracellular Ca2+ signalling plays a major regulatory role in stimulating wound healing, however, the mechanism whereby
injury increases Ca2+ levels at the wound edge is still unclear. The analysis of Ca2+ signals elicited by scraping an
endothelial monolayer in vitro suggested the involvement of intracellular Ca2+ release from InsP3-sensitive stores and Ca2+
entry through unknown ion channels in the plasma membrane. Recent studies carried out on excised rat aorta highlighted
a novel role for connexin hemichannels (CxHcs) in mediating Ca2+ entry in injured endothelium. Understanding the signal
transduction pathway leading to EC activation is likely to provide novel targets to design therapeutic applications aiming
to restore endothelial integrity and treat cardiovascular diseases. Therefore, alternative drug-eluting stents might be
devised to trigger CxHc opening and reduce in-stent restenosis following vascular regenerative surgery.