Objective: Protein kinase B2 (AKT2) is implicated in cardiomyocyte survival during various stress conditions. However, the role of AKT2 in heart function, cardiac hypertrophy and blood pressure (BP) control during hypertension is not fully understood. Therefore, we sought to determine whether the deletion of AKT2 protects cardiac function during angiotensin II/high-salt-diet (AngII/HSD) treatment and find out the signaling pathway. Methods: Male C57BL/6J (wild type), AKT2 knockout and interleukin (IL)-6 knockout mice were fed a 4% NaCl diet for 5 weeks. In the last week, mice were split in two groups and infused subcutaneously with either vehicle or AngII (1.5 μg/h per mouse) for 1 week. Then, BP and cardiac function were assessed. Immunohistology of IL-6 and monocyte chemoattractant protein 1 was performed to detect inflammation in the heart. Masson's trichrome staining was performed to evaluate cardiac fibrosis. Heart tissue homogenates and neonatal mice cardiomyocytes were collected to analyze oxidative stress. Results: Compared with wild-type mice, AKT2 knockout mice maintained BP and showed better left ventricle ejection fraction, lower level of fibrosis, reduced oxidative stress, reduced IL-6 expression and less macrophage infiltration, when treated with AngII/HSD. IL-6 knockout mice treated with AngII/HSD also showed alleviated left ventricular function, fibrosis, oxidative stress and macrophage infiltration compared with wild type. Conclusion: AKT2 deficiency prevents the development of AngII/HSD-induced hypertension, cardiac dysfunction and myocardial injury including oxidative stress, fibrosis and inflammation by suppressing IL-6 expression. These data reveal an important role of the AKT2-IL-6 pathway in mediating AngII/HSD-induced hypertension and cardiomyopathy.

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乐备实是国内专注于提供高质量蛋白检测以及组学分析服务的实验服务专家，自2018年成立以来，乐备实不断寻求突破，公司的服务技术平台已扩展到单细胞测序、空间多组学、流式检测、超敏电化学发光、Luminex多因子检测、抗体芯片、PCR Array、ELISA、Elispot、PLA蛋白互作、多色免疫组化、DSP空间多组学等30多个，建立起了一套涵盖基因、蛋白、细胞以及组织水平实验的完整检测体系。

 
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