Fig. 6: Kat2a aggravated ferroptosis by enhancing Tfrc and Hmox1 expression. | Cell Death & Disease

Fig. 6: Kat2a aggravated ferroptosis by enhancing Tfrc and Hmox1 expression.

From: Histone acetyltransferase Kat2a regulates ferroptosis via enhancing Tfrc and Hmox1 expression in diabetic cardiomyopathy

Fig. 6

A The mRNA expression levels of Kat2a, Tfrc, and Hmox1 were assessed in Kat2a-depleted NMVCs with overexpression of either Tfrc or Hmox1 (N = 3 independent experiments). B The cell death of Kat2a-depleted NMVCs with overexpression of either Tfrc or Hmox1 (N = 3 independent experiments). C The level of labile iron in Kat2a-depleted NMVCs with overexpression of either Tfrc or Hmox1 (N = 3 independent experiments). D The level of lipid ROS in Kat2a-depleted NMVCs with overexpression of either Tfrc or Hmox1 (N = 3 independent experiments). E The level of MDA in Kat2a-depleted NMVCs with overexpression of either Tfrc or Hmox1 (N = 3 independent experiments). F, G GSH and GSH/GSSG levels in Kat2a-depleted NMVCs with overexpression of either Tfrc or Hmox1 (N = 3 independent experiments). H The mRNA expression levels of Kat2a, Tfrc, and Hmox1 were assessed in Kat2a-overexpressing NMVCs with knockdown of either Tfrc or Hmox1 (N = 3 independent experiments). I The cell death of Kat2a-overexpressing NMVCs with knockdown of either Tfrc or Hmox1 (N = 3 independent experiments). J The level of labile iron in Kat2a-overexpressing NMVCs with knockdown of either Tfrc or Hmox1 (N = 3 independent experiments). K The level of lipid ROS in Kat2a-overexpressing NMVCs with knockdown of either Tfrc or Hmox1 (N = 3 independent experiments). L The level of MDA in Kat2a-overexpressing NMVCs with knockdown of either Tfrc or Hmox1 (N = 3 independent experiments). M, N GSH and GSH/GSSG levels in Kat2a-overexpressing NMVCs with knockdown of either Tfrc or Hmox1 (N = 3 independent experiments). Significance tested using One-way ANOVA. Statistical significance is shown as *p < 0.05, **p < 0.01, ***p < 0.001.

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