ArticleJournal of the American Society of Nephrology : JASN2011
Mast cells mediate acute kidney injury through the production of TNF.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Protective Effect of Mannitol on Cisplatin-Induced Nephrotoxicity: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Assessment of pH-Responsive Ionisable Lipid Nanoparticles as Cisplatin Delivery Vehicles for Treating Cisplatin-Resistant Ovarian Cancer.Pharmaceutics · 2026Article
- Immunological mechanisms and novel therapeutic strategies for sepsis‑associated acute kidney injury (Review).International journal of molecular medicine · 2026Review
- Immune microenvironment in autosomal dominant polycystic kidney disease.Genes & diseases · 2026Review
- Navigating the Ethereal Tightrope: The Nanogenerator Manipulates Neurons for Immune Equilibrium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Article
- Role of Mast Cells and Their Mediators in Chronic Kidney Diseases.International journal of molecular sciences · 2025Review
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Neutrophil extracellular traps-related genes contribute to sepsis-associated acute kidney injury.BMC nephrology · 2025Article
- Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.BMC nephrology · 2025Review
- Neutralizing the Th1 effector cytokines, IFN-γ and TNF-α, attenuates established experimental autoimmune anti-myeloperoxidase glomerulonephritis.Frontiers in immunology · 2025Article
- Review
- Lymphocytes and innate immune cells in acute kidney injury and repair.Nature reviews. Nephrology · 2024Review
- Comprehensive analysis of cuproptosis-related genes in immune infiltration and development of a novel diagnostic model for acute kidney injury.Renal failure · 2024Article
- Degranulation of Murine Resident Cochlear Mast Cells: A Possible Factor Contributing to Cisplatin-Induced Ototoxicity and Neurotoxicity.International journal of molecular sciences · 2023Article
- Analysis and Verification of Glycosylation Characteristics of Septic Acute Kidney Injury.Journal of inflammation research · 2023Article
- Gasdermin D-deficient mice are hypersensitive to acute kidney injury.Cell death & disease · 2022Article
- Mast cell tissue heterogeneity and specificity of immune cell recruitment.Frontiers in immunology · 2022Review
- The Role of Vascular-Immune Interactions in Modulating Chemotherapy Induced Neuropathic Pain.Frontiers in pharmacology · 2022Article
- Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury.Frontiers in medicine · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukocyte recruitment contributes to acute kidney injury (AKI), but the mechanisms by which leukocytes promote injury are not completely understood. The degranulation of mast cells releases inflammatory molecules, including TNF, but whether these cells participate in the pathogenesis of AKI is unknown. Here, we induced AKI with cisplatin in mast cell-deficient and wild-type mice. Compared with wild-type mice, deficiency of mast cells attenuated renal injury, reduced serum levels of TNF, and reduced recruitment of leukocytes to the inflamed kidney. Mast cell-deficient mice also exhibited significantly lower intrarenal expression of leukocyte chemoattractants. Mast cell-deficient mice reconstituted with mast cells from wild-type mice exhibited similar cisplastin-induced renal damage and serum levels of TNF as wild-type mice. In contrast, mast cell-deficient mice reconstituted with mast cells from TNF-deficient mice continued to demonstrate significant attenuation of cisplatin-induced renal injury. Furthermore, the mast-cell stabilizer sodium chromoglycate also significantly abrogated renal injury in this model of AKI. Taken together, these results suggest that mast cells mediate AKI through the production of TNF.
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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.