Vascular smooth muscle cells (VSMCs) can undergo phenotypic
modulation (PM) to a dedifferentiated state, which contributes to
angiogenesis and vessel repair. PM is triggered by vascular surgeries such
as those directed to unclog obstructed vessels. However, an excessive
VSMC migration and proliferation drives intimal hyperplasia (IH) leading to
restenosis. This situation is even worse in patients with background
diseases like type 2 diabetes mellitus (T2DM). T2DM patients have more
aggressive forms of vascular disease and worse outcomes, with
exacerbated restenosis after vascular surgery.
We have previously demonstrated that an increased functional expression
of the potassium channel Kv1.3 contributes to PM in several models of
VSMCs, as Kv1.3 blockers inhibit VSMCs migration and proliferation. In
addition, we found that Kv1.3 increased activity upon PM is a consequence
of Kv1.5 downregulation, so that the changes in Kv1.3 to Kv1.5 ratio can
define VSMCs phenotype.
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