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The only-defect group failed to regenerate during the experimental period, and the defect sites injected either nave or GSH-low hES-MSCs were partly filled with cartilage for 12 weeks (Fig

found that ferroptosis was non-cell-autonomously regulated by E-cadherin-mediated intercellular interactions, which repressed ferroptosis by activating intracellular NF2 (neurofibromin 2)-YAP (Yes1-associated transcriptional regulator) signaling[96]

Di Domenico F, Tramutola A, Foppoli C, Head E, Perluigi M, Butterfield DA (2018) mTOR in Down syndrome: role in A and tau neuropathology and transition to Alzheimer disease-like dementia

doi:10.1056/NEJMoa2001180