Why the study?
Does inhibition of Gbetagamma-mediated signaling prevent vascular smooth muscle proliferation and intimal hyperplasia in experimental models of vascular disease?
Does inhibition of Gbetagamma-mediated signaling prevent vascular smooth muscle proliferation and intimal hyperplasia in experimental models of vascular disease?
Targeting Gbetagamma-mediated signaling pathways may offer a novel therapeutic approach to prevent restenosis and vein-graft failure following coronary interventions.
Summary Proliferation of vascular smooth muscle (VSM) severely affects theoutcomeofcoronaryarterybypassandangioplastyprocedures, causing the failure of venous grafts or restenosis of the reopened vessel. Investigation intothemechanisms underlying theprocess of VSMcellularproliferationhasprovidedevidencethatintracellular signaling mechanisms triggered by extracellular hormonal factors acting through G protein‐coupled receptors, can mediate and sustain this pathological process. Inhibition of common pathways of G protein‐coupled receptor signaling has recently proven effective in preventing VSM cellular activation and proliferation. In particular, inhibition of the G¯°-mediated mitogen-activated protein (MAP) kinase signaling pathway results in the inhibition of VSM proliferationinvitro.Moreover,use ofadenoviralvectors todeliver a peptide inhibitor of G¯° signaling in vivo has resulted in inhibition of intimal hyperplasia in experimental models of vein-graft failure and restenosis. IUBMBLife, 48: 257‐261, 1999
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Iaccarino et al. (1999) studied this question.
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