ArticleBritish journal of pharmacology2020
Metabolic reprogramming by N-acetyl-seryl-aspartyl-lysyl-proline protects against diabetic kidney disease.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 66 citations in OpenAlex.
- The Role of Glycolysis in Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- AMPK is dispensable for physiological podocyte and glomerular functions but prevents glomerular fibrosis in experimental diabetes.Cell death discovery · 2026Article
- Kidney angiopoietin-like protein 4 regulates fibrotic responses in diabetic kidney disease.Frontiers in pharmacology · 2026Review
- Article
- Sirtuin 3 in diabetic kidney disease: mechanisms and pharmacotherapy.Renal failure · 2025Review
- Metabolic reprogramming by endothelial ANGPTL4 depletion protects against diabetic kidney disease.bioRxiv : the preprint server for biology · 2025Article
- Editorial: Diabetic kidney disease: routes to drug development, pharmacology and underlying molecular mechanisms, volume II.Frontiers in pharmacology · 2025Article
- The molecular determinants regulating redox signaling in diabetic endothelial cells.Frontiers in pharmacology · 2025Review
- Baicalin: a potential therapeutic agent for acute kidney injury and renal fibrosis.Frontiers in pharmacology · 2025Review
- Landscape analysis of m6A modification regulators reveals LRPPRC as a key modulator in tubule cells for DKD: a multi-omics study.Frontiers in pharmacology · 2025Article
- Editorial: Identification of effective biomarkers for diagnosis and treatment of chronic kidney disease: integrating bioinformatics and pharmacological approaches.Frontiers in pharmacology · 2025Article
- Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease.Science advances · 2024Article
- Unraveling Diabetic Kidney Disease: The Roles of Mitochondrial Dysfunction and Immunometabolism.Kidney international reports · 2024Review
- Mitochondrial metabolic reprogramming in diabetic kidney disease.Cell death & disease · 2024Review
- HOXD10 attenuates renal fibrosis by inhibiting NOX4-induced ferroptosis.Cell death & disease · 2024Article
- (Pro)renin receptor mediates tubular epithelial cell pyroptosis in diabetic kidney disease via DPP4-JNK pathway.Journal of translational medicine · 2024Article
- FGF21 ameliorates diabetic nephropathy through CDK1-dependently regulating the cell cycle.Frontiers in pharmacology · 2024Article
- Sirtuins in kidney homeostasis and disease: where are we now?Frontiers in endocrinology · 2024Review
- Abnormal Expression of Prolyl Oligopeptidase (POP) and Its Catalytic Products Ac-SDKP Contributes to the Ovarian Fibrosis Change in Polycystic Ovary Syndrome (PCOS) Mice.Biomedicines · 2023Article
- Editorial: Receptor biology and cell signaling in diabetes: volume II.Frontiers in pharmacology · 2023Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeACE inhibitors (ACEIs) and AT EXPERIMENTAL APPROACH: Male diabetic CD-1 mice were treated with ACEI, ARB, N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), ACEI + AcSDKP, ARB + AcSDKP, glycolysis inhibitors or non-treatment. Moreover, prolyl oligopeptidase inhibitor (POPi)-injected male diabetic C57Bl6 mice were treated with ACEI, AcSDKP and ARB or non-treatment. Western blot and immunofluorescent staining were used to examine key enzymes and regulators of central metabolism. KEY
resultsThe antifibrotic action of ACEI imidapril is due to an AcSDKP-mediated antifibrotic mechanism, which reprograms the central metabolism including restoring SIRT3 protein and mitochondrial fatty acid oxidation and suppression of abnormal glucose metabolism in the diabetic kidney. Moreover, the POPi S17092 significantly blocked the AcSDKP synthesis, accelerated kidney fibrosis and disrupted the central metabolism. ACEI partly restored the kidney fibrosis and elevated the AcSDKP level, whereas the ARB (TA-606) did not show such effects in the POPi-injected mice. ACE inhibition and AcSDKP suppressed defective metabolism-linked mesenchymal transformations and reduced collagen-I and fibronectin accumulation in the diabetic kidneys. CONCLUSION AND IMPLICATIONS: The study envisages that AcSDKP is the endogenous antifibrotic mediator that controls the metabolic switch between glucose and fatty acid metabolism and that suppression of AcSDKP leads to disruption of kidney cell metabolism and activates mesenchymal transformations leading to severe fibrosis in the diabetic kidney.
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