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• W2572471946 abstract "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" @default.
• W2572471946 created "2017-01-26" @default.
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• W2572471946 date "1999-09-01" @default.
• W2572471946 modified "2023-09-23" @default.
• W2572471946 title "Gbetagamma-Mediated Signaling: New Therapeutic Target for Proliferative Vascular Disease" @default.
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• W2572471946 doi "https://doi.org/10.1080/152165499306937" @default.
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