ArticleLaboratory investigation; a journal of technical methods and pathology2014
Activation of platelet-activating factor receptor exacerbates renal inflammation and promotes fibrosis.
Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
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- Platelet-Activating Factor Pathway in Women With Metabolic Dysfunction-Associated Steatotic Liver Disease and Obesity.Obesity (Silver Spring, Md.) · 2026Article
- Laminin α5: a key factor in tumor metastasis.Clinical & experimental metastasis · 2025Review
- An AI-assisted morphoproteomic approach is a supportive tool in esophagitis-related precision medicine.EMBO molecular medicine · 2025Article
- G protein-coupled receptor-mediated renal fibrosis: a key focus on kidney disease drug development.Frontiers in pharmacology · 2025Review
- Differential expression of serum TM, PAF, and CD62P in patients with autologous arteriovenous fistula and the correlation with vascular access function.Immunity, inflammation and disease · 2024Article
- Localized cardiac small molecule trajectories and persistent chemical sequelae in experimental Chagas disease.Nature communications · 2023Article
- Platelets in Renal Disease.International journal of molecular sciences · 2023Review
- The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis.Journal of hematology & oncology · 2022Review
- The Role of Platelets in Diabetic Kidney Disease.International journal of molecular sciences · 2022Review
- miR‑200b upregulation promotes migration of BEAS‑2B cells following long‑term exposure to cigarette smoke by targeting ETS1.Molecular medicine reports · 2021Article
- ROS‑mediated hypomethylation of PRDX5 promotes STAT3 binding and activates the Nrf2 signaling pathway in NSCLC.International journal of molecular medicine · 2021Article
- Association between changes in the mRNA expression of platelet-activating factor receptor in peripheral blood mononuclear cells and progression of diabetic nephropathy.Diabetology international · 2020Article
- Systemic Platelet-Activating Factor-Receptor Agonism Enhances Non-Melanoma Skin Cancer Growth.International journal of molecular sciences · 2018Article
- Inflammation, not Cholesterol, Is a Cause of Chronic Disease.Nutrients · 2018Review
- LncRNA PFL contributes to cardiac fibrosis by acting as a competing endogenous RNA of let-7d.Theranostics · 2018Article
- UPLC/Q-TOFMS-Based Metabolomics Approach to Reveal the Protective Role of Other Herbs in An-Gong-Niu-Huang Wan Against the Hepatorenal Toxicity of Cinnabar and Realgar.Frontiers in pharmacology · 2018Article
- Epithelial-mesenchymal transition (EMT): A biological process in the development, stem cell differentiation, and tumorigenesis.Journal of cellular physiology · 2017Review
- Tracing the dynamics of gene transcripts after organismal death.Open biology · 2017Article
- Contribution of the platelet activating factor signaling pathway to cerebral microcirculatory dysfunction during experimental sepsis by ExoU producing Pseudomonas aeruginosa.Pathogens and disease · 2015Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet-activating factor (PAF) is a lipid mediator with important pro-inflammatory effects, being synthesized by several cell types including kidney cells. Although there is evidence of its involvement in acute renal dysfunction, its role in progressive kidney injury is not completely known. In the present study, we investigated the role of PAF receptor (PAFR) in an experimental model of chronic renal disease. Wild-type (WT) and PAFR knockout (KO) mice underwent unilateral ureter obstruction (UUO), and at kill time, urine and kidney tissue was collected. PAFR KO animals compared with WT mice present: (a) less renal dysfunction, evaluated by urine protein/creatinine ratio; (b) less fibrosis evaluated by collagen deposition, type I collagen, Lysyl Oxidase-1 (LOX-1) and transforming growth factor β (TGF-β) gene expression, and higher expression of bone morphogenetic protein 7 (BMP-7) (3.3-fold lower TGF-β/BMP-7 ratio); (c) downregulation of extracellular matrix (ECM) and adhesion molecule-related machinery genes; and (d) lower levels of pro-inflammatory cytokines. These indicate that PAFR engagement by PAF or PAF-like molecules generated during UUO potentiates renal dysfunction and fibrosis and might promote epithelial-to-mesenchymal transition (EMT). Also, early blockade of PAFR after UUO leads to a protective effect, with less fibrosis deposition. In conclusion, PAFR signaling contributes to a pro-inflammatory environment in the model of obstructive nephropathy, favoring the fibrotic process, which lately will generate renal dysfunction and progressive organ failure.
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