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In DN renal tissues, mitochondrial accumulation due to dysfunction can be clearly observed, indicating that mitochondrial damage plays a significant role in ferroptosis during DN (143)

Immune dysfunction Since one of the most supported hypotheses for the origin of ME/CFS is bacterial or viral (85, 99, 444) infection (94)

It has a long cyclic half-life and exhibits excellent antidementia activity in scopolamine and aged rat models and marked synaptogenic activity [13,14]

4

Both decreases and increases in reduced glutathione (GSH) and glutathione disulfide (GSSG) levels were reported in fibroblasts undergoing senescence, including replicative senescence (RS), oncogene-induced senescence (OIS), and therapy-induced senescence (TIS) (Quijano et al., 2012