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The impact of changed redoxin function on ferroptosis could also be based on secondary effects, e.g., the increase in superoxide formation upon loss of mitochondrial redoxins [90,91] or activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway [92,93] , a major regulator of transcription of antioxidant and anti-ferroptotic enzymes [65]

Specifically, the authors found that acute glycolytic inhibition increased glutathione and pyruvate metabolism

Healing Injuries: Stem cell therapy can accelerate the healing process for shoulder joint injuries, including those affecting the rotator cuff, tendons, and cartilage

Targeting iron metabolism Low iron levels restrict ferroptosis and result in chemoresistance, while elevated LIPs enhance ferroptosis susceptibility

Wnt/-catenin signaling plays a distinct role in methyl gallate-mediated inhibition of adipogenesis