ArticleJournal of the American Society of Nephrology : JASN2016
Competing Actions of Type 1 Angiotensin II Receptors Expressed on T Lymphocytes and Kidney Epithelium during Cisplatin-Induced AKI.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Effects of proximal tubule-specific ATRAP enhancement on hypertension in a remnant kidney chronic kidney disease model of mice.Scientific reports · 2025Article
- Article
- Review
- Cisplatin treatment reduces contraction to angiotensin II by altering expression of angiotensin II receptors: a pilot study.Molecular and cellular biochemistry · 2023Article
- Long-Term Effects of Severe Burns on the Kidneys: Research Advances and Potential Therapeutic Approaches.Journal of inflammation research · 2023Review
- Angiotensin II enhances bacterial clearance via myeloid signaling in a murine sepsis model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Endoplasmic reticulum stress contributes to cisplatin-induced chronic kidney disease via the PERK-PKCδ pathway.Cellular and molecular life sciences : CMLS · 2022Article
- Type 1 Angiotensin Receptors on CD11c-Expressing Cells Protect Against Hypertension by Regulating Dendritic Cell-Mediated T Cell Activation.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Associations of High-Sensitivity Troponin and Natriuretic Peptide Levels With Serious Adverse Events in SPRINT.Journal of the American Heart Association · 2022Article
- PP2Acα promotes macrophage accumulation and activation to exacerbate tubular cell death and kidney fibrosis through activating Rap1 and TNFα production.Cell death and differentiation · 2021Article
- DNA demethylase Tet2 suppresses cisplatin-induced acute kidney injury.Cell death discovery · 2021Article
- Review
- Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion.Scientific reports · 2021Article
- Immunomodulatory Effects of Mesenchymal Stem Cells on Drug-Induced Acute Kidney Injury.Frontiers in immunology · 2021Review
- Angiotensin (1-7) Attenuates Sepsis-Induced Acute Kidney Injury by Regulating the NF-κB Pathway.Frontiers in pharmacology · 2021Article
- Animal Models of Renal Pathophysiology and Disease.Methods in molecular biology (Clifton, N.J.) · 2021Article
- The transcription factor Twist1 in the distal nephron but not in macrophages propagates aristolochic acid nephropathy.Kidney international · 2020Article
- Integrated Analysis of m6A Methylome in Cisplatin-Induced Acute Kidney Injury and Berberine Alleviation in Mouse.Frontiers in genetics · 2020Article
- Novel Variants of Angiotensin Converting Enzyme-2 of Shorter Molecular Size to Target the Kidney Renin Angiotensin System.Biomolecules · 2019Article
- Opposing actions of renal tubular- and myeloid-derived porcupine in obstruction-induced kidney fibrosis.Kidney international · 2019Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Inappropriate activation of the renin-angiotensin system (RAS) contributes to many CKDs. However, the role of the RAS in modulating AKI requires elucidation, particularly because stimulating type 1 angiotensin II (AT1) receptors in the kidney or circulating inflammatory cells can have opposing effects on the generation of inflammatory mediators that underpin the pathogenesis of AKI. For example, TNF-α is a fundamental driver of cisplatin nephrotoxicity, and generation of TNF-α is suppressed or enhanced by AT1 receptor signaling in T lymphocytes or the distal nephron, respectively. In this study, cell tracking experiments with CD4-Cre mT/mG reporter mice revealed robust infiltration of T lymphocytes into the kidney after cisplatin injection. Notably, knockout of AT1 receptors on T lymphocytes exacerbated the severity of cisplatin-induced AKI and enhanced the cisplatin-induced increase in TNF-α levels locally within the kidney and in the systemic circulation. In contrast, knockout of AT1 receptors on kidney epithelial cells ameliorated the severity of AKI and suppressed local and systemic TNF-α production induced by cisplatin. Finally, disrupting TNF-α production specifically within the renal tubular epithelium attenuated the AKI and the increase in circulating TNF-α levels induced by cisplatin. These results illustrate discrepant tissue-specific effects of RAS stimulation on cisplatin nephrotoxicity and raise the concern that inflammatory mediators produced by renal parenchymal cells may influence the function of remote organs by altering systemic cytokine levels. Our findings suggest selective inhibition of AT1 receptors within the nephron as a promising intervention for protecting patients from cisplatin-induced nephrotoxicity.
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