ReviewMediators of inflammation2015
Proinflammatory Cytokines and Potassium Channels in the Kidney.
Review in Mediators of inflammation, 2015. 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, 19 citations in OpenAlex.
- The critical role of ion channels in kidney disease: perspective from AKI and CKD.Renal failure · 2025Review
- Article
- The impact of tubular dysfunction and its relationship with acute kidney injury in children.Pediatric nephrology (Berlin, Germany) · 2024Article
- Formerly bile-farmed bears as a model of accelerated ageing.Scientific reports · 2023Article
- The Anti-diabetic Drug Gliquidone Modulates Lipopolysaccharide-Mediated Microglial Neuroinflammatory Responses by Inhibiting the NLRP3 Inflammasome.Frontiers in aging neuroscience · 2021Article
- Review on Biological Characteristics of Kv1.3 and Its Role in Liver Diseases.Frontiers in pharmacology · 2021Review
- Early life stress induces immune priming in kidneys of adult male rats.American journal of physiology. Renal physiology · 2018Article
- Protein Kinase R Mediates the Inflammatory Response Induced by Hyperosmotic Stress.Molecular and cellular biology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proinflammatory cytokines affect several cell functions via receptor-mediated processes. In the kidney, functions of transporters and ion channels along the nephron are also affected by some cytokines. Among these, alteration of activity of potassium ion (K(+)) channels induces changes in transepithelial transport of solutes and water in the kidney, since K(+) channels in tubule cells are indispensable for formation of membrane potential which serves as a driving force for the transepithelial transport. Altered K(+) channel activity may be involved in renal cell dysfunction during inflammation. Although little information was available regarding the effects of proinflammatory cytokines on renal K(+) channels, reports have emerged during the last decade. In human proximal tubule cells, interferon-γ showed a time-dependent biphasic effect on a 40 pS K(+) channel, that is, delayed suppression and acute stimulation, and interleukin-1β acutely suppressed the channel activity. Transforming growth factor-β1 activated KCa3.1 K(+) channel in immortalized human proximal tubule cells, which would be involved in the pathogenesis of renal fibrosis. This review discusses the effects of proinflammatory cytokines on renal K(+) channels and the causal relationship between the cytokine-induced changes in K(+) channel activity and renal dysfunction.
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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.