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Subsequent studies showed that in vertebrates, most soluble hydrolases are trafficked by the cation-dependent and cation-independent mannose 6-phosphate (M6P) receptors, CDMPR and CIMPR

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Metabolites such as trimethylamine N-oxide (TMAO) and homocysteine derivatives exacerbate endothelial injury, while gut microbiome interactions further modulate disease progression