ArticleKidney3602022
F4/80
Article in Kidney360, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Embryonic and postnatal macrophages are necessary for proper tooth development and homeostasis.Nature communications · 2026Article
- ELMO1 dependent efferocytosis protects from nephrotoxin induced acute kidney injury.Cell death discovery · 2026Article
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- ALKBH5 induces macrophage activation to promote renal fibrosis via Retnla.Renal failure · 2025Article
- Polymer-based chemo-immunotherapy: Combining immunogenic cell death induction and PD-L1 blockade enhances antitumor immunity in melanoma.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- Exercise sensitizes the pressure diuresis response: shifting immune landscapes may underlie renal adaptations.American journal of physiology. Renal physiology · 2025Article
- Tissue-resident macrophages and renal diseases: landscapes and treatment directions.Frontiers in immunology · 2025Review
- Macrophage depletion protects against cisplatin-induced ototoxicity and nephrotoxicity.Science advances · 2024Article
- Polyamine Catabolism and Its Role in Renal Injury and Fibrosis in Mice Subjected to Repeated Low-Dose Cisplatin Treatment.Biomedicines · 2024Article
- Macrophages polarization in renal inflammation and fibrosis animal models (Review).Molecular medicine reports · 2024Review
- Myeloid-derived Wnts play an indispensible role in macrophage and fibroblast activation and kidney fibrosis.International journal of biological sciences · 2024Article
- Macrophage Depletion Protects Against Cisplatin-Induced Ototoxicity and Nephrotoxicity.bioRxiv : the preprint server for biology · 2023Article
- The impact of hypoxia-inducible factors in the pathogenesis of kidney diseases: a link through cell metabolism.Kidney research and clinical practice · 2023Article
- Tissue transglutaminase exacerbates renal fibrosis via alternative activation of monocyte-derived macrophages.Cell death & disease · 2023Article
- Lung cancer-kidney cross talk induces kidney injury, interstitial fibrosis, and enhances cisplatin-induced nephrotoxicity.American journal of physiology. Renal physiology · 2023Article
- Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation.Frontiers in medicine · 2023Article
- Macrophage promotes fibroblast activation and kidney fibrosis by assembling a vitronectin-enriched microenvironment.Theranostics · 2023Article
- Resident macrophage subpopulations occupy distinct microenvironments in the kidney.JCI insight · 2022Article
- Pharmacological inhibitors of autophagy have opposite effects in acute and chronic cisplatin-induced kidney injury.American journal of physiology. Renal physiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Background: Cisplatin-induced kidney injury remains a major obstacle in utilizing cisplatin as a chemotherapeutic for solid-organ cancers. Thirty percent of patients treated with cisplatin develop acute kidney injury (AKI), and even patients who do not develop AKI are at risk for long-term declines in kidney function and development of chronic kidney disease (CKD). Modeling cisplatin-induced kidney injury in mice has revealed that repeated low doses of cisplatin lead to development of kidney fibrosis. This model can be used to examine AKI-to-CKD transition processes. Macrophages play a role in some of these processes, including immune response, wound healing, and tissue remodeling. Depleting macrophage populations in the kidney reduced fibrosis development in other models of renal fibrosis. Methods: We used either C57BL/6 mice with a Ccr2 genetic knockout or liposome encapsulated clodronate (Clodrosome) to deplete macrophage populations during repeated 9 mg/kg cisplatin treatments. We assessed how immune cell populations were altered in the blood and kidney of these mice and how these alterations affected development of renal fibrosis and kidney injury. Results: We found that Clodrosome treatment decreased collagen deposition, myofibroblast accumulation, and inflammatory cytokine production, whereas Ccr2 genetic knockout had no effect on these markers after cisplatin treatment. Additionally, Ccr2 Conclusions: These data suggest that Clodrosome depletion of F4/80
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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.