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Tat and Tat-Cocaine treatment induce neuronal damage, which is mitigated by 4OI through microglia cells

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Efforts should be made to promote a shift from merely alleviating symptoms to truly disease-modifying treatment strategies that protect joint structure and function, thereby providing a new theoretical basis and translational direction for precise intervention in OA

The concurrent activation of HACD44 and GSHNrf2 signaling axes establishes a dual regulatory network that synchronizes inflammation resolution with oxidative stress mitigation, fostering an optimal biochemical niche for rapid and organized wound closure