Key result
Targeting renal ANGPTL4 reduces diabetic kidney fibrosis by modulating lipid metabolism and inflammation.
This review highlights ANGPTL4 as a critical mediator of fibrosis and inflammation in diabetic kidney disease, suggesting it as a promising therapeutic target.
May implicate hyposialylated ANGPTL4 in diabetic kidney fibrosis; leaves open targeted therapies for clinical trials.
The angiopoietin-like (ANGPTL) proteins are now recognized as critical regulators of the harmful changes seen in diabetic kidney disease. Notably, a hyposialylated pro-proteinuric form of ANGPTL4 has been identified as a crucial contributor to fibrosis within diabetic kidneys. Under diabetic conditions, glomerular podocytes secrete this hyposialylated ANGPTL4, which plays a significant role in disrupting lipid metabolism, promoting inflammation, and driving fibrosis in both podocytes and adjacent tubules. This secreted ANGPTL4 interacts with tubular cells via Integrin-1 and DPP-4, causing mitochondrial damage that activates the c-GAS-STING pathway and exacerbates inflammation. Importantly, targeting renal ANGPTL4 with antisense oligonucleotides (ASOs) has shown promising protective effects against fibrosis in diabetic kidneys, paving the way for innovative therapeutic strategies to combat diabetic kidney disease and other fibrotic disorders.
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Srivastava et al. (2026) conducted a review in Diabetic kidney disease. ANGPTL4 inhibition was evaluated. Targeting renal ANGPTL4 with antisense oligonucleotides shows promising protective effects against fibrosis in diabetic kidneys by modulating lipid metabolism and inflammation.
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