Figure 9: Summary of the mechanisms of ferroptosis in HD and ferroptosis as a therapeutic ...

Summary of the mechanisms of ferroptosis in HD and ferroptosis as a therapeutic target for HD. Frequent cleavage of mHTT leads to the formation of toxic aggregates, accompanied by reductions in GSH and GPX4, and increased ionic accumulation, ultimately resulting in mitochondrial damage and neuronal degeneration. Iron chelators such as DFO, DFP, and DFX have been shown to reduce iron overload, attenuate LPO, and improve mitochondrial function. QCT exerts neuroprotective effects in HD by targeting SIRT1, thereby mitigating mHTT-mediated inhibition. In addition, mHTT aggregates induce neuroinflammation by suppressing the Nrf2 signaling pathway. Creatine (Cr), through its active form PCr, participates in the CK-mediated ADP–ATP cycle, alleviating oxidative stress in mitochondria. Together with CoQ10, Cr helps reduce mitochondrial ROS accumulation. HDAC inhibitors enhance the acetylation of the transcription factor Sp1 and upregulate SOD1, GPX4, and catalase, thereby counteracting oxidative

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