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NNMT promotes tubular senescence and fibrosis in chronic kidney disease

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE280554 | GEO | 2025/11/20

REPOSITORIES: GEO

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NNMT overexpression promotes tubular senescence and fibrosis in human chronic kidney disease (Nnmt overexpressing TEC cells) [Series_3]

Project description:Renal tubular epithelial cells (TECs) are increasingly recognized as the central locus of chronic kidney disease and renal fibrosis. Here, we used conditionally immortalized TECs (expressing SV40 large T antigen at permissive conditions, 33°C with IFNγ, and behaving like normal primary cultures after 7 days in restrictive conditions, 37°C without IFNγ) and genetically overexpressed Nnmt (Nnmt-OE) by means of lentiviral transduction of a mock or Nnmt expression construct. In the TGFβ model mimicking the senescent and pro-fibrotic changes in TECs, Nnmt overexpression resulted in an aggravated phenotype.

2025-11-20 | GSE280552 | GEO

NNMT overexpression promotes tubular senescence and fibrosis in human chronic kidney disease (NNMT inhibition in TEC cells) [Series_1]

Project description:Renal tubular epithelial cells (TECs) are increasingly recognized as the central locus of chronic kidney disease and renal fibrosis. Here, we used conditionally immortalized TECs (expressing SV40 large T antigen at permissive conditions, 33°C with IFNγ, and behaving like normal primary cultures after 7 days in restrictive conditions, 37°C without IFNγ), stimulated with TGFβ to mimic the senescent and pro-fibrotic phenotypic shift of TECs during kidney disease. Co-treating the cells with the selective and membrane-permeable small molecule 5-amino-1-methylquinolinium iodide (NNMTi) significantly protected against senescence and epithelial-to-mesenchymal transition in TGFβ-stimulated TECs.

2025-11-20 | GSE280542 | GEO

NNMT promotes tubular senescence and fibrosis in chronic kidney disease

Project description:NNMT promotes tubular senescence and fibrosis in chronic kidney disease

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NNMT promotes tubular senescence and fibrosis in chronic kidney disease (db/m and db/db mice kidney)

Project description:Diabetic kidney disease is the leading cause of chronic kidney disease. db/db mice, which carry a deletion mutation resulting in a dysfunctional leptin receptor, exhibit hyperphagia, obesity, and elevated insulin levels, making them a widely used preclinical model of diabetic kidney disease. At 16 weeks of age, db/db mice showed enriched transcriptomic signatures of cellular senescence in their kidneys compared to control db/m mice.

2025-11-20 | GSE283610 | GEO

NNMT overexpression promotes tubular senescence and fibrosis in human chronic kidney disease (NNMT inhibition and SAM supplementation in TEC cells)

Project description:Renal tubular epithelial cells (TECs) are increasingly recognized as the central locus of chronic kidney disease and renal fibrosis. Here, we used conditionally immortalized TECs (expressing SV40 large T antigen at permissive conditions, 33°C with IFNγ, and behaving like normal primary cultures after 7 days in restrictive conditions, 37°C without IFNγ), stimulated with TGFβ to mimic the senescent and pro-fibrotic phenotypic shift of TECs during kidney disease. TGFβ stimulation and co-treatment with either the small-molecule NNMT inhibitor 5-amino-1-methylquinolinium iodide (NNMTi) or S-adenosyl methionine (SAM) altered the DNA methylation profile of the cells.

2025-11-20 | GSE310712 | GEO

NNMT overexpression promotes tubular senescence and fibrosis in human chronic kidney disease (young, old and NAM-supplemented old mice kidney) [Series_4]

Project description:Aging is a major risk factor for chronic kidney disease. Aged mice (21 months old) exhibited enriched transcriptomic signatures of fibrosis and cellular senescence in their kidneys compared to young mice (4 months old), and dietary supplementation with nicotinamide (NAM) was insufficient to reverse these disease signatures.

2025-11-20 | GSE280553 | GEO

NNMT overexpression promotes tubular senescence and fibrosis in human chronic kidney disease (NAM and SAM supplementation in TEC cells) [Series_2]

Project description:Renal tubular epithelial cells (TECs) are increasingly recognized as the central locus of chronic kidney disease and renal fibrosis. Here, we used conditionally immortalized TECs (expressing SV40 large T antigen at permissive conditions, 33°C with IFNγ, and behaving like normal primary cultures after 7 days in restrictive conditions, 37°C without IFNγ), stimulated with TGFβ to mimic the senescent and pro-fibrotic phenotypic shift of TECs during kidney disease. Co-treating the cells with nicotinamide (NAM) did not prevent the senescence and epithelial-to-mesenchymal transition in TGFβ-stimulated TECs, while co-treating with S-adenosyl methionine (SAM) attenuated this dysfunctional phenotype.

2025-11-20 | GSE280551 | GEO

Tubular cell senescence promotes maladaptive kidney repair and chronic kidney disease after cisplatin nephrotoxicity.

Project description:Cisplatin is a widely used chemotherapy drug; however, it induces both acute and chronic kidney diseases (CKD) in patients with cancer. The pathogenesis of cisplatin-induced CKD is unclear, and effective renoprotective approaches are not available. Here, we report that repeated low-dose cisplatin (RLDC) treatment of C57BL/6 mice induced chronic cellular senescence in kidney tubules, accompanied with tubular degeneration and profibrotic phenotype transformation that culminated in maladaptive repair and renal fibrosis. Suppression of tubular senescence by senolytic drugs ABT-263 and Fisetin attenuated renal fibrosis and improved tubular repair, as indicated by restoration of tubular regeneration and renal function. In vitro, RLDC also induced senescence in mouse proximal tubular (BUMPT) cells. ABT-263 eliminated senescent BUMPT cells following RLDC treatment, reversed the profibrotic phenotype of the cells, and increased their clonogenic activity. Moreover, ABT-263 alleviated the paracrine effect of RLDC-treated BUMPT cells on fibroblasts for fibrosis. Consistently, knockdown of p16 suppressed post-RLDC senescence and fibrotic changes in BUMPT cells and alleviated their paracrine effects on renal fibroblast proliferation. These results indicate that persistent induction of tubular senescence plays an important role in promoting cisplatin-induced CKD. Targeting senescent tubular cells may be efficient for improvement of kidney repair and for the prevention and treatment of cisplatin-induced CKD.

| S-EPMC10243740 | biostudies-literature

NNMT overexpression promotes tubular senescence and fibrosis in human chronic kidney disease (Nnmt overexpressing TEC cells) [Series_3]

Project description:NNMT overexpression promotes tubular senescence and fibrosis in human chronic kidney disease (Nnmt overexpressing TEC cells) [Series_3]

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Integrin β3 Induction Promotes Tubular Cell Senescence and Kidney Fibrosis.

Project description:Tubular cell senescence is a common biologic process and contributes to the progression of chronic kidney disease (CKD); however, the molecular mechanisms regulating tubular cell senescence are poorly understood. Here, we report that integrin β3 (ITGB3) expression was increased in tubular cells and positively correlated with fibrosis degree in CKD patients. ITGB3 overexpression could induce p53 pathway activation and the secretion of TGF-β, which, in turn, resulted in senescent and profibrotic phenotype change in cultured tubular cells. Moreover, according to the CMAP database, we identified isoliquiritigenin (ISL) as an agent to inhibit ITGB3. ISL treatment could suppress Itgb3 expression, attenuate cellular senescence, and prevent renal fibrosis in mice. These results reveal a crucial role for integrin signaling in cellular senescence, potentially identifying a new therapeutic direction for kidney fibrosis.

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