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Enhanced Ca(2+)-channeling complex formation at the ER-mitochondria interface underlies the pathogenesis of alcohol-associated liver disease

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Despite reperfusion reestablishing oxygenation, it paradoxically exacerbates the injury by promoting reactive oxygen species production and encouraging pro-inflammatory neutrophils to infiltrate the ischemic tissues, thereby amplifying the ischemic damage [49] (Fig

(A) Fractional enrichment of label from 15 N 4 -arginine in intracellular arginine pools following 18 hour incubation in tracer-containing HPLM of NHA Donor #1 stable lines expressing either empty vector (EV), wild-type AGAT cDNA (AGAT WT), or catalytically-dead AGAT cDNA (AGAT C407A) and Cas9 with either an sgRNA targeting the AAVS1 safe-harbor locus control or one of two sgRNAs targeting GAMT