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Specifically, recent research has suggested a bidirectional communication between metabolic dysfunction (loss of metabolic homeostasis) and cellular senescence (67, 68)

In addition, loss of glutathione peroxidase 4 (GPX4), a central regulator of ferroptosis, leads to hemolytic anemia and increases spleen erythroid progenitor death through receptor-interacting protein 3 (RIP3)-dependent necroptosis signaling 48

Chiou, Senile cataracts and oxidative stress

The reduction in SAM tissue concentrations resulting from the altered homocysteine remethylation might be compensated for by the increase in SAM synthesis with the methionine supply (Miller et al, 1994a)

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