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[51] revealed that IGF-1 significantly downregulated the PI3K/Akt signaling pathway, cell adhesion/endothelial stromal cell receptor pathway, T and B cell signaling pathway, and cytokines storm and inflammatory factors

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doi: 175

110 Despite a number of studies that reported somewhat conflicting results regarding the different cardiac phenotypes in response to increased AKT activity, it has currently been recognized that short-term appropriate AKT activation leads to physiological cardiac hypertrophy, while long-term AKT activation or AKT overexpression causes pathological cardiac hypertrophy, interstitial fibrosis, and even heart failure

Although an inflammatory phenotype was not detected in the brain, systemic immune dysregulation was suggested by significant decreases of IFN, TNF, IL-1, and IL10 (Zakirova et al., 2017)