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Thyrnosin-beta 4-mediated therapeutic neovascularization: role of the PI3K/AKT pathway

机译:胸腺素β4介导的治疗性新血管形成:PI3K / AKT途径的作用

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Objectives: Thymosin beta 4 (T beta 4) is known to have pro-angogenic abilities in vitro and in vivo, and its cardioprotective effect is PI3/AKT-dependent. T beta 4-induced vessel formation requires transcriptional activation via the MRTF/SRF pathway. However, the relevance of PI3/AKT signaling for T beta 4-induced angiogenesis remains unclear. Here, we analyzed the PI3K/AKT cascade after T beta 4 transduction in models of chronic hindlimb ischemia.
机译:目的:胸腺素β4(Tβ4)在体外和体内均具有促血管生成的能力,其心脏保护作用是PI3 / AKT依赖性的。 Tβ4诱导的血管形成需要通过MRTF / SRF途径进行转录激活。但是,PI3 / AKT信号传导与T beta 4诱导的血管生成的相关性仍不清楚。在这里,我们分析了慢性后肢缺血模型中T beta 4转导后的PI3K / AKT级联。

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