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Before the surge of genetic evidence supporting the association of NMDAR malfunction with schizophrenia, hypofunction of NMDARs in the pathogenesis of schizophrenia was originally identified from observations on the psychotomimetic effects of non-competitive NMDAR antagonists

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In AKI, metabolic stress elevates glycerol-3-phosphate (G3P) in the renal cortex, which is transported to the bone marrow and converted to LPA via GPAT2