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To understand why senescent cells are more prone than normal counterparts to undergo ferroptosis on GPX4 inhibition, we used fluorescence probes to analyse ROS, levels of Fe 2+ and lipid oxidation in senescent cells

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This work was supported by the Wilmot Cancer Institute Predoctoral Fellowship (G.A.), Wilmot Cancer Institute Pilot Funding (I.S.H.), the American Association for Cancer Research and Breast Cancer Research Foundation (20-20-26-HARR) (I.S.H.), Breast Cancer Coalition of Rochester (I.S.H.), a Sir Henry Wellcome Postdoctoral Fellowship (M.E.K.), and a FNR-CORE grant C21/BM/15796788 (D.B.), and NIH grants R01CA269813 (I.S.H.), R37CA230042 (G.M.D), R24AA022057 (V.V.), R01AA028859 (Y.C.), AI150698 (J.M.), K01CA240533-01A1 (C.L.C.), and R01AR078000 (R.T.D.)

The most actionable approach is tracking the downstream markers that respond to glutathione status: oxidative stress markers, liver enzymes, methylation markers, and inflammation