ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Accelerated Glomerular Cell Senescence in Experimental Lupus Nephritis.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Withaferin A, a candidate drug for lupus nephritis, confers renal protection via Pon1‑mediated attenuation of oxidative stress.International journal of molecular medicine · 2026Article
- Identification of cellular senescence-related genes as biomarkers for lupus nephritis based on bioinformatics.Frontiers in genetics · 2025Article
- Inflammasome activation and accelerated immune aging in autoimmune disorders.Frontiers in aging · 2025Article
- Targeting cellular senescence in kidney diseases and aging: A focus on mesenchymal stem cells and their paracrine factors.Cell communication and signaling : CCS · 2024Review
- Inhibition of receptor interacting protein kinase-1 (RIPK1) in the treatment of murine lupus.Lupus science & medicine · 2024Article
- Cellular senescence and kidney aging.Clinical science (London, England : 1979) · 2023Review
- p16Lupus science & medicine · 2023Article
- Metformin improves renal injury of MRL/lpr lupus-prone mice via the AMPK/STAT3 pathway.Lupus science & medicine · 2022Article
- Hydroxychloroquine administration exacerbates acute kidney injury complicated by lupus nephritis.Arthritis research & therapy · 2022Article
- High p16RMD open · 2021Article
- Dexamethasone reduces autoantibody levels in MRL/lpr mice by inhibiting Tfh cell responses.Journal of cellular and molecular medicine · 2021Article
- Brahma-related gene-1 promotes tubular senescence and renal fibrosis through Wnt/β-catenin/autophagy axis.Clinical science (London, England : 1979) · 2021Article
- Lansoprazole promotes cisplatin-induced acute kidney injury via enhancing tubular necroptosis.Journal of cellular and molecular medicine · 2021Article
- Accumulation of Senescent Neural Cells in Murine Lupus With Depression-Like Behavior.Frontiers in immunology · 2021Article
- IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis.Frontiers in immunology · 2021Review
- Cellular Senescence: A New Player in Kidney Injury.Hypertension (Dallas, Tex. : 1979) · 2020Review
- The emerging role of cellular senescence in renal diseases.Journal of cellular and molecular medicine · 2020Review
- Blast Exposure Leads to Accelerated Cellular Senescence in the Rat Brain.Frontiers in neurology · 2020Article
- Role of p300 in the pathogenesis of Henoch-Schonlein purpura nephritis and as a new target of glucocorticoid therapy in mice.Chinese medical journal · 2019Article
- Cell Senescence in Lupus.Current rheumatology reports · 2019Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to determine whether senescence in renal glomeruli is involved in lupus nephritis (LN); the expression of senescence-associated β-galactosidase (SA-β-Gal) and its association with glomerular lesions were investigated in a mouse model of LN. MATERIAL AND METHODS Eighteen MRL/lpr mice with severe proteinuria were randomly divided into 2 equal groups and intraperitoneally injected with dexamethasone (DEX) or saline; 4 age-matched mice with mild proteinuria served as controls. Serum creatinine and urinary protein levels were analyzed, and kidney histological changes were observed by periodic acid-Schiff and Sirius Red staining. SA-β-Gal was detected via histochemistry. Glomerular expression of collagen IV, α-SMA, and nephrin was analyzed by immunohistochemistry, and glomerular complement C3 deposition was tested by immunofluorescence. The relationships between SA-β-Gal expression and renal function or glomerular lesion markers were determined by Spearman's correlation analysis. RESULTS Mice with severe proteinuria exhibited glomerular segmental sclerosis and endothelial cell proliferation. DEX administration suppressed these lesions but had no significant effect on 24-hour urinary protein levels. The elevated glomerular expression of SA-β-Gal in proteinuric mice was attenuated by DEX treatment. In addition, DEX treatment markedly downregulated glomerular C3 deposition and collagen IV and α-SMA expression, while significantly increasing nephrin expression. Furthermore, SA-β-Gal expression was positively correlated with urinary protein levels and expression of α-SMA. CONCLUSIONS Accelerated senescence of glomerular cells may contribute to glomerular injury in LN.
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