ArticleBMB reports2019
Tissue-resident natural killer cells exacerbate tubulointerstitial fibrosis by activating transglutaminase 2 and syndecan-4 in a model of aristolochic acid-induced nephropathy.
Article in BMB reports, 2019. 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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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- The Endothelial Glycocalyx: The First Line of Defense in the Prevention and Treatment of Kidney Diseases.Kidney medicine · 2025Review
- Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease.Nature reviews. Nephrology · 2025Review
- APP-CD74 axis mediates endothelial cell-macrophage communication to promote kidney injury and fibrosis.Frontiers in pharmacology · 2024Article
- Amino acid metabolism in immune cells: essential regulators of the effector functions, and promising opportunities to enhance cancer immunotherapy.Journal of hematology & oncology · 2023Review
- Natural Killer Cells, as the Rising Point in Tissues, Are Forgotten in the Kidney.Biomolecules · 2023Review
- Syndecan-4 as a Marker of Endothelial Dysfunction in Patients with Resistant Hypertension.Journal of clinical medicine · 2020Article
- Sirtuin 1 and endothelial glycocalyx.Pflugers Archiv : European journal of physiology · 2020Review
- Recent Advances in the Role of Natural Killer Cells in Acute Kidney Injury.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite reports suggesting that tissue-resident natural killer (trNK) cells cause ischemic kidney injury, their contribution to the development of tubulointerstitial fibrosis has not been determined. This study hypothesized that the depletion of trNK cells may ameliorate renal fibrosis by affecting transglutaminase 2/syndecan-4 interactions. Aristolochic acid nephropathy (AAN) was induced in C57BL/6 mice as an experimental model of kidney fibrosis. The mice were treated with anti-asialo GM1 (ASGM1) or anti-NK1.1 antibodies to deplete NK cells. Although both ASGM1 and NK1.1 antibodies suppressed renal NKp46
Indexed as
Identifiers
31072444PMC6774424W2978992918What 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.