Rather being an inert barrier between vessel lumen and surrounding tissues, vascular endothelium
plays a key role in the maintenance of cardiovascular homeostasis. The de-endothelialization of blood vessels
is regarded as the early event that results in the onset of severe vascular disorders, including atherosclerosis,
acute myocardial infarction, brain stroke, and aortic aneurysm. Restoration of the endothelial lining may be
accomplished by the activation of neighbouring endothelial cells (ECs) freed by contact inhibition and by
circulating endothelial progenitor cells (EPCs). Intracellular Ca2+ signalling is essential to promote wound
healing: however, the molecular underpinnings of the Ca2+ response to injury are yet to be fully elucidated.
Similarly, the components of the Ca2+ toolkit that drive EPC incorporation into denuded vessels are far from
being fully elucidated. The present review will survey the current knowledge on the role of Ca2+ signalling in
endothelial repair and in EPC activation. We propose that endothelial regeneration might be boosted by
intraluminal release of specific Ca2+ channel agonists or by gene transfer strategies aiming to enhance the
expression of the most suitable Ca2+ channels at the wound site. In this view, connexin (Cx)
channels/hemichannels and store-operated Ca2+ entry (SOCE) stand amid the most proper routes to
therapeutically induce the regrowth of denuded vessels. Cx stimulation might trigger the proliferative and
migratory behaviour of ECs facing the lesion site, whereas activation of SOCE is likely to favour EPC homing
to the wounded vessel.
Keywords: Ca2+signalling, Ca2+ oscillations, connexin hemichannels, endothelial dysfunction, endothelial
progenitor cells, ischemic disease, Orai1, Stim1, TRPC1.
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