ArticleWorld journal of diabetes2025
Nicotinamide mononucleotide protects against diabetic nephropathy
Article in World journal of diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Glomerulo-Tubular Crosstalk in Diabetic Kidney Disease: From Pathophysiology to Novel Therapeutics.Electrolyte & blood pressure : E & BP · 2026Review
- Exploring novel pathways and potential therapeutic targets for diabetic nephropathy: The interplay of podocytes and proximal tubular epithelial cells.World journal of diabetes · 2026Article
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3 authors.
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Abstract
backgroundDiabetic nephropathy (DN) is a leading cause of chronic kidney disease and end-stage renal disease, and is a significant global healthcare burden. Although proximal tubular epithelial cells (PTECs) and podocytes are involved in DN progression, the specific molecular interactions between these cells are not well understood.
aimTo elucidate the role of interleukin-6 (IL-6)/Rab5 signaling in mediating crosstalk between PTECs and podocytes, and to evaluate the protective effects of nicotinamide mononucleotide (NMN) against DN progression.
methodsWe utilized
resultsHigh-glucose conditions induced the epithelial-mesenchymal transition (EMT) in PTECs, increased IL-6 secretion, and activated Rab5 signaling in podocytes, leading to increased nephrin endocytosis and podocyte injury. Blocking IL-6 significantly attenuated these effects. NMN treatment of diabetic mice markedly reduced podocyte injury, glomerular hypertrophy, foot-process effacement, and urinary albumin excretion. Mechanistically, NMN suppressed the EMT and IL-6 secretion by PTECs, inhibited Rab5 activation in podocytes, and prevented nephrin endocytosis, thereby preserving the cytoskeletal integrity and function of podocytes.
conclusionOur findings reveal a novel pathogenic mechanism of DN in which IL-6 released from glucose-stressed PTECs activates Rab5 signaling in podocytes, followed by nephrin endocytosis and structural injury of podocytes. Importantly, NMN treatment effectively disrupted this pathological pathway of intercellular communication, and provided significant protection against DN progression. These results suggest that NMN supplementation and targeting the IL-6/Rab5 signaling axis has promise as a therapeutic strategy for managing DN.
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