ArticleCirculation research2025
Podocyte NPRC Deficiency Attenuates Glomerular Fibrosis in Diabetic Mice.
Article in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Natriuretic peptide receptor C in cardiovascular-kidney-liver-metabolic syndrome: from natriuretic peptide deficiency to direct tissue signaling?Reviews in endocrine & metabolic disorders · 2026Review
- Podocyte specific knockout (KO) of the natriuretic peptide clearance receptor (NPRC) attenuates diabetic kidney disease (DKD).Physiological reports · 2026Article
- Lipid metabolism drives podocyte injury in diabetic kidney disease.Frontiers in immunology · 2026Review
- Wnt5a-mediated Adipo-Cardiac Interorgan Communication in HFpEF.bioRxiv : the preprint server for biology · 2025Article
- Salvaged Signals, Scarred Filters: Podocyte NPRC in Diabetic Kidney Disease.Circulation research · 2025Article
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15 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundRenal fibrosis plays a key role in the progression of diabetic kidney disease (DKD). Although the renal protective effects of NPs (natriuretic peptides) were reported, the role of NPR (natriuretic peptide receptor) C in modulating renal fibrosis in DKD remains unclear.
methodsThe expression and function of NPRC in DKD were investigated using human renal biopsies and a diabetic mouse model. Podocyte-specific NPRC knockout mice were developed to explore the role of NPRC in renal fibrosis. Gene and protein analyses such as histological staining, serum chemical assay, mass spectrometry analysis, ELISA, and Western blot were performed to examine the impact of NPRC deficiency on TGF-βR (transforming growth factor-β receptor) 2 expression, recycling, small mothers against decapentaplegic homolog 2/3 (Smad2/3) signaling, and the overall renal structure and function.
resultsIncreased expression of NPRC was observed in both patients with DKD and DKD mice. Podocyte-specific NPRC knockout mice showed reduced glomerular fibrosis and improved podocyte injury and renal function compared with wild-type controls. Notably, NPRC knockdown resulted in decreased COL (collagen) synthesis in podocytes. Molecular biology studies revealed that NPRC deficiency led to decreased recycling and increased degradation of TGF-βR2, thus suppressing the TGF-β (transforming growth factor-β)1/Smad pathway.
conclusionsNPRC plays a detrimental role in the progression of DKD by enhancing TGF-βR2 expression and TGF-β1/Smad signaling pathway. Podocyte-specific NPRC deficiency not only attenuates glomerular fibrosis but also improves renal function, suggesting that NPRC may serve as a promising therapeutic target for managing diabetic renal fibrosis.
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