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Increased Gb3 expression and lipid accumulation in GLA-KO human iPSC kidney organoids Next, to determine the accumulation of Gb3, a main pathological mechanism in human Fabry disease 6,7 , confocal microscopy was performed, which revealed extensive accumulation of Gb3 in podocytes and tubular cells in GLA-mutant human iPSC kidney organoids (Fig

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H 2 S is involved in mitochondrial functioning, insulin sensitivity, lipoprotein synthesis, and glucose metabolism in the liver [6]