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Demonstrating that ferroptosis is a driver of disease in CF offers the opportunity to intervene therapeutically and in this study we showed that the GSH prodrug N-acetylcysteine (NAC) was able to recover the levels of GSH back to normal and alleviate erastin-induced ferroptotic cell death

under normal conditions, BDNF binds to TrkB receptors to activate pathways such as ERK and Akt, activating the mammalian target of rapamycin complex 1 (mTORC1), which drives synaptic protein synthesis, promoting dendritic spine and synapse formation, and maintaining synaptic structures (118)

Point mutations in Arf1 reveal cooperative effects of the N-terminal extension and myristate for GTPase-activating protein catalytic activity

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At present, how to avoid or reduce the damage to sperm quality caused by a high-altitude environment has become an important topic worthy of in-depth study