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observed a marked increase in ACSL4 expression in a heart failure model induced by TAC in mice, and ACSL4 overexpression in cardiomyocytes exacerbates the cardiac dysfunction triggered by pressure overload through ferroptosis

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In combination with the classical study showing that S-phase cells in normal rat tissues did not tend to exhibit Txr immunostaining (Hansson et al., 1986), there is a good possibility that the GSH system is supporting RNR activity in TrxR1-deficient hepatocytes (Holmgren and Sengupta, 2010)