ArticleRenal failure2021
Effect of galectin-3 in the pathogenesis of arteriovenous fistula stenosis formation.
Article in Renal failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Fibroblast growth factor 21 predicts arteriovenous fistula functional patency loss and mortality in patients undergoing maintenance hemodialysis.Renal failure · 2024Article
- Galectin-3: action and clinical utility in chronic kidney disease.International urology and nephrology · 2024Review
- Building a Scaffold for Arteriovenous Fistula Maturation: Unravelling the Role of the Extracellular Matrix.International journal of molecular sciences · 2023Review
- The potential roles of galectin-3 in AKI and CKD.Frontiers in physiology · 2023Review
- Increased expression of the P2YRenal failure · 2023Article
Corrections and comments
- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study sought to investigate the effect of local expression of galectin-3 in the development of stenotic arteriovenous fistula (AVF).
methodsWe collected stenotic venous tissues, adjacent nonstenotic venous tissues, and blood samples from end-stage renal disease (ESRD) patients with AVF stenosis, while normal venous tissues and blood samples were collected from ESRD patients before AVF creation as controls. Also blood samples were collected from ESRD patients with nonstenosis functional AVF. Galectin-3, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase-9 (MMP-9), and α-SMA expression in the venous tissues were examined by immunohistochemistry, and the ERK1/2 pathway activity in the intima was accessed by western blot. Serum galectin-3 level was measured by ELISA. Thereafter, human pulmonary arterial smooth muscle cells (HPASMCs) were cultured
resultsESRD patients with stenotic AVF had a significant higher serum galectin-3 level than normal controls, and patients with non-stenotic functional AVF. The expression levels of galectin-3, phosphorylated ERK1/2, PCNA, MMP-9, and α-SMA in the stenotic venous tissues were higher than that in the normal venous tissues or the adjacent nonstenotic AVF venous tissues. Correlation analysis showed that the expression of galectin-3 of the neointima was positively correlated with PCNA and α-SMA in the stenotic AVF venous tissues. In HPASMCs, galectin-3 can increase the activity of phosphorylated ERK1/2 and promote the expression of α-SMA.
conclusionIn the stenotic AVF of ESRD patients, expression of the galectin-3 was significantly increased, showing a positive relation with neointima development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.