ArticleJournal of the American Society of Nephrology : JASN2011
Blocking Fas ligand on leukocytes attenuates kidney ischemia-reperfusion injury.
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 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Plant metabolites: potential treatments for ischemic acute kidney injury.Frontiers in pharmacology · 2026Review
- Diagnostic PANoptosis-related genes in acute kidney injury: bioinformatics, machine learning, and validation.Annals of medicine · 2025Article
- Multiomic analysis of human kidney disease identifies a tractable inflammatory and pro-fibrotic tubular cell phenotype.Nature communications · 2025Article
- Molecular Mechanisms and Potential Therapeutic Targets of Ischemia-Reperfusion Injury in Kidney Transplantation.Current issues in molecular biology · 2025Review
- Methyl-CpG-binding domain protein 2 contributes to renal fibrosis through promoting polarized M1 macrophages.Cell death & disease · 2022Article
- Type 1 Innate Lymphoid Cells Are Proinflammatory Effector Cells in Ischemia-Reperfusion Injury of Steatotic Livers.Frontiers in immunology · 2022Article
- Expanded renal lymphatics improve recovery following kidney injury.Physiological reports · 2021Article
- Fas ligand neutralization attenuates hypertension, endothelin-1, and placental inflammation in an animal model of HELLP syndrome.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Carbon monoxide protects the kidney through the central circadian clock and CD39.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Tumor necrosis factor superfamily ligand mRNA expression profiles differ between humans and mice during homeostasis and between various murine kidney injuries.Journal of biomedical science · 2017Article
- Novel Therapies for Acute Kidney Injury.Kidney international reports · 2017Review
- Circulating levels of soluble Fas (sCD95) are associated with risk for development of a nonresolving acute kidney injury subphenotype.Critical care (London, England) · 2017Article
- Kidney-specific Sonoporation-mediated Gene Transfer.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Hypoxia-Inducible Factor-2α Limits Natural Killer T Cell Cytotoxicity in Renal Ischemia/Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2016Article
- Associations between single nucleotide polymorphisms in the FAS pathway and acute kidney injury.Critical care (London, England) · 2015Article
- Immune cells in experimental acute kidney injury.Nature reviews. Nephrology · 2015Review
- The role of lymphocytes in the development and treatment of alopecia areata.Expert review of clinical immunology · 2015Review
- Renal atrophy after ischemia-reperfusion injury depends on massive tubular apoptosis induced by TNFα in the later phase.Medical molecular morphology · 2014Article
- Regulated cell death and inflammation: an auto-amplification loop causes organ failure.Nature reviews. Immunology · 2014Article
- Necroptosis.The New England journal of medicine · 2014Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation contributes to the pathogenesis of ischemic acute kidney injury (AKI), and T cells mediate the early phase of ischemia-reperfusion injury (IRI). The Fas/Fas ligand (FasL) pathway modulates the balance of T cell subsets in the peripheral circulation as well as multiple inflammatory responses, suggesting that FasL may mediate ischemic AKI. Here, we induced bilateral renal IRI in mice bearing a loss-of-function mutation of FasL (the gld mutation) and in wild-type mice. Compared with wild-type mice, serum creatinine was lower in gld mice (1.4 ± 0.9 mg/dl versus 2.6 ± 0.4) at 24 hours after IRI (P<0.05). In addition, gld mice had fewer TNF-α-producing T lymphocytes in the kidneys and renal lymph nodes. Furthermore, pharmacologic blockade of FasL protected the kidneys of wild-type mice from IRI. Analysis of bone marrow chimeric mice suggested that the pathogenic effect of FasL involves leukocytes; reconstitution of wild-type mice with gld splenocytes attenuated IRI. In contrast, reconstitution of gld mice with wild-type splenocytes enhanced IRI. These data demonstrate that FasL, particularly on leukocytes, mediates ischemic AKI.
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Registered trials
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