Inhibition of human in-stent restenosis: a molecular view

The current management of the stenosis of the coronary arteries relies on the insertion of a metal mesh tube, namely stent, into the obstructed vessel. Coronary stents have been envisaged to reduce the restenosis after balloon angioplasty. Nonetheless, one of the major complications after successful revascularization is the late in-stent restenosis. Such lesion consists mainly of inflammatory reaction and neointima formation as a consequence of the mechanical injury of the vessel. In this review, we examine the molecular players underlying the in-stent restenosis, with particular reference to the role of the mTOR pathway and the intracellular receptor immunophilins. The ‘limus’ based drugs, which are developed or are under development in drug-eluting stent technology, will be also discussed.

► The pharmacological modulation of mTOR pathway is critical on controlling restenosis post-coronary angioplasty.
► Immunophilins are fundamental determinants of limus drug action.
► Limus-inhibitors of calcineurin phosphatase are ineffective on controlling the cell proliferation post-coronary angioplasty.
► Among the mTOR inhibitors, additional therapeutic differences may rely upon the involvement of supplementary molecular partners as FKBP51.