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Treating cells with L-buthionine sulfoximine (BSO), an inhibitor that blocks the synthesis of GSH, renders neuronal SH-SY5Y cells expressing mutant valosin-containing protein (VCP) R487H more susceptible to oxidative stress (Hirano et al., 2015) and increases mutant SOD1 toxicity (Alvarez-Zaldiernas et al., Drosophila models increases markers of oxidative stress, including protein carbonylation and glutathione S transferase D1 (Duan et al., 2010

Such attempts play along with green chemistry and circular economy ideals

Through activation of the VEGFR2/PI3K/AKT pathway, VEGF stimulates synovial fibroblast proliferation and invasion, exemplified by MH7A cells, ultimately driving pathological synovial tissue thickening

doi: 10.1067/mcp.2000.104736