ArticleAmerican journal of physiology. Renal physiology2018
Interleukin 1 receptor (IL-1R1) activation exacerbates toxin-induced acute kidney injury.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 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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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Protective role of Boerhavia diffusa root extract in methotrexate-induced renal injury: evidence from oxidative stress, molecular, and immunohistochemical markers.BMC complementary medicine and therapies · 2026Article
- Urine Proteomics as a Source of Biological Information and Outcome Predictor in Living Kidney Transplantation.Molecular & cellular proteomics : MCP · 2026Article
- Low-intensity pulsed ultrasound stimulation to treat renal fibrosis through inhibiting tubular IL-1R.JCI insight · 2025Article
- Research progress on damage-associated molecular patterns in acute kidney injury.Frontiers in immunology · 2025Review
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Targeting interleukin-1 signaling for renoprotection.Frontiers in immunology · 2025Review
- Baicalin: a potential therapeutic agent for acute kidney injury and renal fibrosis.Frontiers in pharmacology · 2025Review
- Novel anti-inflammatory effects of the IL-1 receptor in kidney myeloid cells following ischemic AKI.Frontiers in molecular biosciences · 2024Article
- Identification and validation of aging-related genes in neuropathic pain using bioinformatics.Frontiers in genetics · 2024Article
- SHED-derived exosomes attenuate trigeminal neuralgia after CCI of the infraorbital nerve in mice via the miR-24-3p/IL-1R1/p-p38 MAPK pathway.Journal of nanobiotechnology · 2023Article
- A macrophage-endothelial immunoregulatory axis ameliorates septic acute kidney injury.Kidney international · 2023Article
- Review
- Ammonium chloride-induced acidosis exacerbates cystitis and pyelonephritis caused by uropathogenic E. coli.Physiological reports · 2022Article
- Lysophosphatidic Acid Is a Proinflammatory Stimulus of Renal Tubular Epithelial Cells.International journal of molecular sciences · 2022Article
- IL-1 receptor signaling in podocytes limits susceptibility to glomerular damage.American journal of physiology. Renal physiology · 2022Article
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- NLRP3 inflammasome in rosmarinic acid-afforded attenuation of acute kidney injury in mice.Scientific reports · 2022Article
- Tetramethylpyrazine: An Active Ingredient of Chinese Herbal Medicine With Therapeutic Potential in Acute Kidney Injury and Renal Fibrosis.Frontiers in pharmacology · 2022Review
- Gasdermin E deficiency attenuates acute kidney injury by inhibiting pyroptosis and inflammation.Cell death & disease · 2021Article
- Metabolic acidosis exacerbates pyelonephritis in mice prone to vesicoureteral reflux.Physiological reports · 2020Article
Corrections and comments
- Erratum issuedCorrigendum.2019
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is a leading cause of morbidity and mortality. Drug-induced/toxic AKI can be caused by a number of therapeutic agents. Cisplatin is an effective chemotherapeutic agent whose administration is limited by significant nephrotoxicity. Therapies to prevent cisplatin-induced AKI are lacking. Although tumor necrosis factor-α (TNF) plays a key role in the pathogenesis of cisplatin nephrotoxicity, the innate immune signaling pathways that trigger TNF generation in this context require elucidation. In this regard, sterile injury triggers the release and activation of both isoforms of interleukin(IL)-1, IL-1α and IL-1β. In turn, stimulation of the interleukin-1 receptor (IL-1R1) by these ligands engages a proinflammatory signaling cascade that induces TNF induction. We therefore hypothesized that IL-1R1 activation exacerbates cisplatin-induced AKI by inducing TNF production, thereby augmenting inflammatory signals between kidney parenchymal cells and infiltrating myeloid cells. IL-1R1+/+ (WT) and IL-1R1-/- (KO) mice were subjected to cisplatin-induced AKI. Compared with WT mice, IL-1R1 KO mice had attenuated AKI as measured by serum creatinine and BUN, renal NGAL mRNA levels, and blinded histological analysis of kidney pathology. In the cisplatin-injured kidney, IL-1R1 KO mice had diminished levels of whole kidney TNF, and fewer Ly6G-expressing neutrophils. In addition, an unbiased machine learning analysis of intrarenal immune cells revealed a diminished number of CD11b
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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.