ArticleKidney international2004
Role of mast cells in the development of renal fibrosis: use of mast cell-deficient rats.
Article in Kidney international, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 66 citations in OpenAlex.
- The mast cell: A Janus in kidney transplants.Frontiers in immunology · 2023Review
- Renal tubular gen e biomarkers identification based on immune infiltrates in focal segmental glomerulosclerosis.Renal failure · 2022Article
- Osteopontin: An important protein in the formation of kidney stones.Frontiers in pharmacology · 2022Review
- A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives.Frontiers in immunology · 2022Review
- Two Sides of the Coin: Mast Cells as a Key Regulator of Allergy and Acute/Chronic Inflammation.Cells · 2021Review
- Mast Cells in Liver Fibrogenesis.Cells · 2019Review
- Biomarkers and the role of mast cells as facilitators of inflammation and fibrosis in chronic kidney disease.Translational andrology and urology · 2019Review
- Delayed Rectifier KBioMed research international · 2019Article
- PAI1 mediates fibroblast-mast cell interactions in skin fibrosis.The Journal of clinical investigation · 2018Article
- Bile duct ligation-induced biliary hyperplasia, hepatic injury, and fibrosis are reduced in mast cell-deficient KitHepatology (Baltimore, Md.) · 2017Article
- Inflammatory processes in renal fibrosis.Nature reviews. Nephrology · 2014Review
- Molecular targets for treatment of kidney fibrosis.Journal of molecular medicine (Berlin, Germany) · 2013Review
- Diabetic nephropathy: the role of inflammation in fibroblast activation and kidney fibrosis.Frontiers in endocrinology · 2013Article
- Lung mast cell density defines a subpopulation of patients with idiopathic pulmonary fibrosis.Histopathology · 2012Article
- Mast cells are required for the development of renal fibrosis in the rodent unilateral ureteral obstruction model.American journal of physiology. Renal physiology · 2012Article
- Mechanistic connection between inflammation and fibrosis.Kidney international. Supplement · 2010Review
- Renal fibrosis: novel insights into mechanisms and therapeutic targets.Nature reviews. Nephrology · 2010Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRecent clinical studies have shown that the number of interstitial mast cells increases in various types of renal disease and correlates well with the magnitude of interstitial fibrosis. The present study was conducted to assess the role of mast cells in renal fibrosis by examining an experimental glomerular disease.
methodsA rat model of chronic glomerular disease, puromycin aminonucleoside-nephrosis, was induced in mast cell-deficient (Ws/Ws) and normal (+/+) rats.
resultsThe area of interstitial fibrosis was widely distributed at 6 weeks in both groups of rats; however, unexpectedly, the area of interstitial fibrosis was greater in Ws/Ws rats than in +/+ littermates. Biochemical analysis of the hydroxyproline content confirmed the more severe fibrosis in the Ws/Ws rats. The number of mast cells increased in both Ws/Ws and +/+ rats, concomitant with the development of interstitial fibrosis, but was confirmed to be lower in Ws/Ws than in +/+ rats. There were no differences in the numbers of interstitial macrophages and T lymphocytes between the two groups. Reverse transcription-polymerase chain reaction analysis of cytokine expression revealed that the level of mRNA for transforming growth factor-beta (TGF-beta), a potent profibrotic cytokine, was higher in Ws/Ws rats. In addition, heparin, one of the major components of mast cells, inhibited the expression of TGF-beta mRNA in rat fibroblasts in culture.
conclusionThese results suggest that mast cells do not play a major role in the pathogenesis of interstitial fibrosis in puromycin aminonucleoside nephrosis. Rather, they might be protective or ameliorative in this model through the inhibition of TGF-beta production by heparin, and possibly in other models and also in humans.
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