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Likewise, there is favorable evidence to support the engraftment of neural stem cells [16] or bone marrow stromal cells [17] into the lesion site

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Under nutrient-excess conditions, sustained leucine elevation drives chronic mTORC1 activation, leading to IRS-1 serine phosphorylation and impaired insulin signaling ( Mitochondrial dysfunction and BCAA accumulation form a bidirectional vicious cycle: impaired oxidative capacity reduces BCAA catabolism, while accumulated intermediates exacerbate mitochondrial stress and ROS generation ( 4.1.3 Clinical evidence and intervention strategies Multiple clinical studies have reported significantly elevated plasma BCAA levels in patients with T2D