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This review critically discusses the potential of ANGPTL4 as a biomarker of DKD and explains mechanistically how does tubule-specific and podocyte-specific ANGPTL4 lead to lipid load, mitochondrial damage, inflammation and defective lipid metabolism, and accumulative effects accelerate the fibrogenesis process in diabetic kidney

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The ability of DMF to downregulate NF-B signaling [36, 37] should not be involved either, as an increase in GST expression is expected following a pharmacological upregulation rather than downregulation of the NF-B pathway, as reported for GST pi [38]

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