ArticleJournal of vascular and interventional radiology : JVIR2011
Expression of profibrotic genes in a murine remnant kidney model.
Article in Journal of vascular and interventional radiology : JVIR, 2011. 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.
The trial behind it
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Egr‑1 promotes the proliferation and migration of vascular smooth muscle cells by transcriptionally activating Egr‑2 in arteriovenous fistulas.International journal of molecular medicine · 2025Article
- Identification and Validation of PTGS2 Gene as an Oxidative Stress-Related Biomarker for Arteriovenous Fistula Failure.Antioxidants (Basel, Switzerland) · 2023Article
- TNFR2 as a Potential Biomarker for Early Detection and Progression of CKD.Biomolecules · 2023Article
- Anti Human CX3CR1 VHH Molecule Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mouse Model.Journal of the American Society of Nephrology : JASN · 2021Article
- MMP-9 Deletion Attenuates Arteriovenous Fistula Neointima through Reduced Perioperative Vascular Inflammation.International journal of molecular sciences · 2021Article
- Therapeutic Effect of Adipose Derived Mesenchymal Stem Cell Transplantation in Reducing Restenosis in a Murine Angioplasty Model.Journal of the American Society of Nephrology : JASN · 2020Article
- The Biology of Hemodialysis Vascular Access Failure.Seminars in interventional radiology · 2016Review
- The molecular mechanisms of hemodialysis vascular access failure.Kidney international · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTo test the hypothesis that there is increased expression of several profibrotic genes, including matrix metalloproteinase (MMP)-2 and MMP-9 and tissue inhibitors of metalloproteinase (TIMP-1 and TIMP-2), a disintegrin and metalloproteinase with thrombospondin motif-1 (ADAMTS-1), and fibroblast specific protein-1 (FSP-1) in a murine remnant kidney model. MATERIALS AND
methodsChronic kidney disease (CKD) was created in 10 C57BL/6 male mice (20-25 g) by performing a right nephrectomy and ligation of the upper pole of the left kidney (remnant kidney). Animals were sacrificed 42 days and 56 days later. Reverse transcriptase polymerase chain reaction (RT-PCR) for MMP-2, MMP-9, TIMP-1, TIMP-2, ADAMTS-1, and FSP-1 was performed in the remnant kidney. Histologic evaluation of the remnant kidney was performed using Ki-67, α-smooth muscle cell actin (α-SMA), hematoxylin and eosin, and Masson' trichrome staining. Kidney function was assessed using serum blood urea nitrogen (BUN) and creatinine.
resultsThe mean serum BUN and creatinine levels at day 42 and day 56 were significantly higher than baseline (P < .05). By day 42, the mean expression of MMP-2, MMP-9, TIMP-1, ADAMTS-1, and FSP-1 was significantly higher in the remnant kidney compared with the normal kidney (P < .05); by day 56, only FSP-1 expression was significantly higher (P < .05). There was increased fibrosis by Masson' trichrome, increased Ki-67, and increased α-SMA staining in the remnant kidney compared with the normal kidney.
conclusionsIn the remnant kidney, there was increased fibrosis with increased α-SMA and Ki-67 staining and significantly increased expression of MMP-2, MMP-9, TIMP-1, ADAMTS-1, and FSP-1.
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