Insulin-like growth factor-1 as a vascular protective factor
Insulin-like growth factor-1 as a vascular protective factor
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DOI：
10.1161/01.cir.0000144309.87183.fb
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发表时间：
2004-10-12
期刊：
影响因子：
37.8
通讯作者：
Andreotti, F
中科院分区：
文献类型：
--
作者：
Conti, E;Carrozza, C;Andreotti, F
Vasodilation by IGF-1 requires NO synthase (NOS) 30 and/or potassium channel activity, 31 dependent on vessel size. 25 In both endothelial cells and VSMCs, 32, 33 IGF-1 increases NOS activity by interacting with a tyrosine kinase membrane receptor linked to the insulin receptor substrate 1 and 2. 34 This receptor complex activates phosphatidylinositol 3-kinase (PI3-K), which activates the serine/threonine kinase Akt signaling pathway. 32, 33 These cascades are downregulated by angiotensin II. 33 Constitutive NOS activity produces a slow, sustained release of NO, with multiple metabolic and vascular-protective effects (Figure 1). These include, in addition to vasodilation, enhanced glucose uptake; reduced gluconeogenesis; antiplatelet actions; free oxygen radical scavenging; endothelial cell migration, proliferation, and survival; and progenitor cell mobilization35 (Figure 1). While increasing constitutive NOS, IGF-1 inhibits inducible NO23, 26; the latter causes large bursts of NO that promote apoptosis and depress myocardial function. 23, 36
