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Studies have shown that the primary reason for this decline is insufficient availability of glycine and cysteine, the amino acids required to build glutathione

Agarwal et al., 2014), the factor H binding protein (fHbp) (Lewis et al., 2012), the sialylation of LOS (Estabrook et al., 1997), and the IgG3 degradation through IgA protease type 1 (Spoerry et al., 2021) protects the meningococcus from complement deposition

LOXL2, a copper-dependent monoamine oxidase, activates lung fibroblasts through the TGF-/Smad pathway

IGF-1 stimulates de novo fatty acid biosynthesis by Schwann cells during myelination

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Current therapeutic strategies mitigate these complications by increasing the concentration of RBCs with normal hemoglobin via transfusion, inducing fetal hemoglobin, restoring nitric oxide signaling, inhibiting platelet-endothelium interaction, and stabilizing hemoglobin in its oxygenated state