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in the future, the combination of specific receptor modulators, molecular targeting, and immune regulation is expected to achieve personalized treatment and precise inflammation control

doi: 10.1186/s13048-022-00962-w Summary Keywords neuroexcitotoxicity, ferroptosis, glutamate, cystine-glutamate antiporter, ischemic stroke Citation Fan G, Liu M, Liu J and Huang Y (2023) The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation

The implication of GST polymorphisms may be significant as studies suggest that that loss of mu, pi and theta GST genes increase susceptibility to inflammatory diseases, and a genetic deficiency of GSTM1 is associated with increased susceptibility to ozone-related asthma [61] and to susceptibility to AFB1-mediated damage to human liver cells [62]