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Fig. 4 Effect of LCM treatment on mitochondria dysfunction in AGTPBP1 KO cells. A Pipeline of glutamate and LCM treatment; B differentiated WT and AGTPBP1 KO cells with vehicle or LCM treatment under control condition (left) or glutamate treatment (right). The difference of cell viability between WT and AGTPBP1 KO cells, n = 12, p < 0.0001. LCM treatment improved survival in AGTPBP1 KO cells, n = 12, p < 0.0001. In glutamate treatment, there was also significant difference in neuronal survival for WT and AGTPBP1 KO cells, n = 12, p = 0.0025. Although LCM treatment did not improve neuronal survival in AGTPBP1 KO cells treated with glutamate, it improved the neuronal survival in WT, n = 12, p = 0.0039. C ROS production. There was a significant difference in ROS production for WT and AGTPBP1 KO cells, n = 12, p = 0.0459. LCM treatment decreased ROS production in AGTPBP1 KO cells, n = 12, p = 0.0268. There was also significant decrease of ROS production in AGTPBP1 KO cells treated with glutamate before and after LCM treatment, n = 12, p = 0.0249; D JC-1 ratio green/red of WT and AGTPBP1 KO cells. Data were presented with normalizing to the ratio of WT *100%, which showed significant difference in two groups, n = 12, p < 0.0001. LCM treatment significantly improved mitochondrial function in AGTPBP1 KO cells, n = 12, p = 0.021. LCM treatment also improved mitochondrial function in WT treated with glutamate, n = 12, p = 0.04. E ATP synthesis recorded by Seahorse, showing improved ATP production in AGTPBP1 KO cells treated with LCM, n = 3, p = 0.0073. *p < 0.05, **p < 0.01, ****p < 0.0001. Data were analyzed by two-way ANOVA, followed by Tukey’s test. Data were presented as mean ± SD