ReviewFrontiers in immunology2016
Mode of Proximal Tubule Damage: Differential Cause for the Release of TFF3?
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 8 citations in OpenAlex.
- The Urinary Concentration of Trefoil Factor 3 (TFF3) in the Term and Preterm Neonates.Journal of clinical medicine · 2023Article
- Pathological and therapeutic roles of bioactive peptide trefoil factor 3 in diverse diseases: recent progress and perspective.Cell death & disease · 2022Review
- Promising biomarkers in pediatric chronic kidney disease through the kaleidoscope of CAKUT background complexity.Pediatric nephrology (Berlin, Germany) · 2021Article
- Renal expression of trefoil factor 3 mRNA in association with tubulointerstitial fibrosis in IgA nephropathy.Nephrology (Carlton, Vic.) · 2018Article
- Urine Trefoil Factors as Prognostic Biomarkers in Chronic Kidney Disease.BioMed research international · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proximal tubular epithelial cells are particularly sensitive to damage. In search of a biomarker, this study evaluated the potential of different cell activation models (hypoxia/replenishment and protein overload) to lead to a release of trefoil factor 3 (TFF3). Surprisingly, we found disparity in the ability of the different stimuli to enhance the intracellular abundance of TFF3 and its release: while conditions of nutrient starvation and damage associated with replenishment lead to intracellular abundance of TFF3 in the absence of TFF3 release, stimulation with an excess amount of albumin did not yield accumulation of TFF3. By contrast, incubation of cells with a purified λ light chain preparation from a patient with multiple myeloma provoked the presence of TFF3 in the cell supernatant. We, therefore, propose that elevations of TFF3 in renal disease might be more revelatory for the cause of restitution than previously thought.
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Registered trials
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