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The tenosynovium (tendon sheath) benefits from enhanced healing while the tendons themselves undergo repair and strengthening

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For example, we have shown that depleting GSH in young wild-type mice results in mitochondrial dysfunction and that correcting GSH deficiency in old wild-type mice lowers reverses mitochondrial impairment, lowers OxS and insulin resistance [29]

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Long-term experience also revealed clinically important limitations

369 Recent studies have demonstrated that neutrophil death in SLE involves ferroptosis, which is characterized by morphological changes such as vacuole formation, disappearance of mitochondrial cristae, and increased membrane density in mitochondria