Notably, in the condition of excess hemin exposure and hypoxia, our findings suggest an important contribution of the TSS pathway and its regulation by DMF for de novo cysteine synthesis and GSH generation in protecting against the oxidative and ferroptotic stresses in SCD erythroblasts
These metabolites regulate intestinal barrier integrity, energy metabolism, and ovarian function by activating the AhR, modulating immune responses (e.g., IL-22), and influencing neuroendocrine pathways (e.g., 5-HT signaling (8587)
Furthermore, the role of p38 MAPK in such diseases has been examined, and its inhibitors are potential therapeutic agents for their treatment [11, 12]
This loss leads to slower waste removal and regeneration processes, accelerating cellular aging