ArticleJournal of clinical medicine2018
CERA Attenuates Kidney Fibrogenesis in the db/db Mouse by Influencing the Renal Myofibroblast Generation.
Article in Journal of clinical medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- New Approaches to Diabetic Nephropathy from Bed to Bench.Biomedicines · 2022Review
- Diabetic fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Effects of Allicin on Pathophysiological Mechanisms during the Progression of Nephropathy Associated to Diabetes.Antioxidants (Basel, Switzerland) · 2020Article
- Advances in Understanding the Effects of Erythropoietin on Renal Fibrosis.Frontiers in medicine · 2020Review
- Recombinant Erythropoietin Provides Protection against Renal Fibrosis in Adenine-Induced Chronic Kidney Disease.Mediators of inflammation · 2020Article
- Anemia in patients of diabetic kidney disease.Journal of the Chinese Medical Association : JCMA · 2019Review
- FoxO1-mediated inhibition of STAT1 alleviates tubulointerstitial fibrosis and tubule apoptosis in diabetic kidney disease.EBioMedicine · 2019Article
- Changes in cell fate determine the regenerative and functional capacity of the developing kidney before and after release of obstruction.Clinical science (London, England : 1979) · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubulointerstitial fibrosis (TIF) is a pivotal pathophysiological process in patients with diabetic nephropathy (DN). Multiple profibrotic factors and cell types, including transforming growth factor beta 1 (TGF-β1) and interstitial myofibroblasts, respectively, are responsible for the accumulation of extracellular matrix in the kidney. Matrix-producing myofibroblasts can originate from different sources and different mechanisms are involved in the activation process of the myofibroblasts in the fibrotic kidney. In this study, 16-week-old
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Registered trials
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