ArticleAmerican journal of physiology. Renal physiology2013
Reactive oxygen species and IRF1 stimulate IFNα production by proximal tubules during ischemic AKI.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 33 citations in OpenAlex.
- Tubule-Derived IFN-α Promotes GSDMD-Mediated Macrophage Pyroptosis to Drive Renal Inflammation and Fibrosis Through JAK2/STAT2 Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Effect of Sodium Thiosulfate Pre-Treatment on Renal Ischemia-Reperfusion Injury in Kidney Transplantation.International journal of molecular sciences · 2024Article
- Increased levels of endogenous retroviruses trigger fibroinflammation and play a role in kidney disease development.Nature communications · 2023Article
- Oxidative stress induces inflammation of lens cells and triggers immune surveillance of ocular tissues.Chemico-biological interactions · 2022Article
- Network-Based Expression Analyses and Experimental Verifications Reveal the Involvement of STUB1 in Acute Kidney Injury.Frontiers in molecular biosciences · 2021Article
- Role of promoting inflammation of Krüppel-like factor 6 in acute kidney injury.Renal failure · 2020Article
- Porous Se@SiOInternational journal of nanomedicine · 2019Article
- NADPH oxidase inhibitor, diphenyleneiodonium prevents necroptosis in HK-2 cells.Biomedical reports · 2017Article
- A Genome-Wide Association Study to Identify Single-Nucleotide Polymorphisms for Acute Kidney Injury.American journal of respiratory and critical care medicine · 2017Article
- Febuxostat exerts dose-dependent renoprotection in rats with cisplatin-induced acute renal injury.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- SIRT2 Regulates LPS-Induced Renal Tubular CXCL2 and CCL2 Expression.Journal of the American Society of Nephrology : JASN · 2015Article
- Macrophage and epithelial cell H-ferritin expression regulates renal inflammation.Kidney international · 2015Article
- Oxidative stress contributes to orthopedic trauma-induced acute kidney injury in obese rats.American journal of physiology. Renal physiology · 2015Article
- Protective effect of epimedium combined with oligomeric proanthocyanidins on exercise-induced renal ischemia-reperfusion injury of rats.International journal of clinical and experimental medicine · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
We previously reported that expression of the transcription factor interferon regulatory factor 1 (IRF1) is an early, critical maladaptive signal expressed by renal tubules during murine ischemic acute kidney injury (AKI). We now show that IRF1 mediates signals from reactive oxygen species (ROS) generated during ischemic AKI and that these signals ultimately result in production of α-subtypes of type I interferons (IFNαs). We found that genetic knockout of the common type I IFN receptor (IFNARI-/-) improved kidney function and histology during AKI. There are major differences in the spatial-temporal production of the two major IFN subtypes, IFNβ and IFNαs: IFNβ expression peaks at 4 h, earlier than IFNαs, and continues at the same level at 24 h; expression of IFNαs also increases at 4 h but continues to increase through 24 h. The magnitude of the increase in IFNαs relative to baseline is much greater than that of IFNβ. We show by immunohistology and study of isolated cells that IFNβ is produced by renal leukocytes and IFNαs are produced by renal tubules. IRF1, IFNαs, and IFNARI were found on the same renal tubules during ischemic AKI. Furthermore, we found that ROS induced IFNα expression by renal tubules in vitro. This expression was inhibited by small interfering RNA knockdown of IRF1. Overexpression of IRF1 resulted in the production of IFNαs. Furthermore, we found that IFNα stimulated production of maladaptive proinflammatory CXCL2 by renal tubular cells. Altogether our data support the following autocrine pathway in renal tubular cells: ROS > IRF1 > IFNα > IFNARI > CXCL2.
Indexed as
Identifiers
What OpenQuestion holds
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.