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At lower concentrations, melittin induces transient relaxation through an endothelium-dependent mechanism involving NO production and activation of smooth muscle charybdotoxin-sensitive K+ channels, but at higher concentrations, it causes contraction

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Activation of these pathways would increase intracellular ROS levels by inhibiting the transcription factor forkhead box transcription factor O (FOXO), which boost the production of antioxidants such as SOD2, catalase, and sestrin3 [28]

SIRT3, a class III HDAC associated with longevity, deacetylates Forkhead box protein O3a (FOXO3a) and promotes transcription of antioxidant enzymes (e.g., manganese superoxide dismutase and catalase), thereby constraining mitochondrial ROS and preserving redox homeostasis [71, 72]

Particular focus should be placed on interactions between mHTT, the ironmetabolism axis (such as transferrin receptor 1 and hepcidin), and key ferroptosis mediators (GPX4 and Nrf2) to build a dynamic model linking mHTT aggregation, iron dysregulation, and neuronal ferroptosis, and to define subtype-specific vulnerability of MSNs