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Diabetic kidney disease (DKD) is characterized by abnormal metabolic profiles. Metabolomics revealed increased serum levels of 3-phosphoglycerate (3-PG) in DKD patients. The protein expression of phosphoglycerate kinase 1 (PGK1), a key rate-limiting enzyme for 3-PG synthesis, was concomitantly upregulated in DKD patients and mice. The development of DKD was significantly mitigated by renal tubular epithelial cell-specific knockout of PGK1 and robustly worsened by PGK1 overexpression. Mechanistically, PGK1-dependent enzymatic production of 3-PG facilitated DKD through inhibiting GPX1 to activate the NLRP3 inflammasome. PGK1 promoted UNC5CL-mediated inflammation by binding with aldehyde dehydrogenase-1 L1 (Aldh1l1) through its non-enzymatic activity. The transcription factor paired box protein 5 (PAX5) mediated the upregulation of PGK1 in DKD. High-throughput screening revealed that C-16 from ChemDiv, the natural product lirinidine, and the FDA-approved Oxantel Pamoate were potent PGK1 antagonists and efficaciously prevented DKD. Overall, blocking PGK1 may be a promising avenue for DKD management. Here, we had put the raw blots (unadjusted and uncropped blots with size markers) and raw stained images for cells in Mendeley.

Western Blot, Staining Technique

Creative Commons Attribution 4.0 International

Diabetic kidney disease (DKD) is characterized by abnormal metabolic profiles. Metabolomics revealed increased serum levels of 3-phosphoglycerate (3-PG) in DKD patients. The protein expression of phosphoglycerate kinase 1 (PGK1), a key rate-limiting enzyme for 3-PG synthesis, was concomitantly upregulated in DKD patients and mice. The development of DKD was significantly mitigated by renal tubular epithelial cell-specific knockout of PGK1 and robustly worsened by PGK1 overexpression. Mechanistically, PGK1-dependent enzymatic production of 3-PG facilitated DKD through inhibiting GPX1 to activate the NLRP3 inflammasome. PGK1 promoted UNC5CL-mediated inflammation by binding with aldehyde dehydrogenase-1 L1 (Aldh1l1) through its non-enzymatic activity. The transcription factor paired box protein 5 (PAX5) mediated the upregulation of PGK1 in DKD. High-throughput screening revealed that C-16 from ChemDiv, the natural product lirinidine, and the FDA-approved Oxantel Pamoate were potent PGK1 antagonists and efficaciously prevented DKD. Overall, blocking PGK1 may be a promising avenue for DKD management. Here, we had put the raw blots (unadjusted and uncropped blots with size markers) and raw stained images for cells in Mendeley.

Western Blot, Staining Technique

Creative Commons Attribution 4.0 International