ArticleHypertension (Dallas, Tex. : 1979)2025
G-CSF Mediates Increased Renal Neutrophils and Kidney Damage in a Psoriasis Mouse Model.
Article in Hypertension (Dallas, Tex. : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- A tissue-engineered human psoriatic skin model: targeting inflammation and glucose metabolism dysregulation in psoriasis using microneedle patches.Frontiers in molecular biosciences · 2026Article
- Deciphering the Underlying Mechanisms Linking Psoriasis and IgA Nephropathy.Journal of immunology research · 2026Review
- Navigating renal safety in the biologic treatment of psoriasis: from immunologic mechanisms to clinical practice.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundPsoriasis is an autoimmune skin disease associated with increased incidence and severity of chronic kidney disease and hypertension. The mechanisms linking psoriasis skin inflammation with these comorbidities remain unclear.
methodsWe used flow cytometry, radiotelemetric blood pressure measurements, and histological and ELISA-based assessments of renal damage in mice with experimental psoriasis induced by keratinocyte-specific
resultsCompared with littermate controls, KC-Tie2 mice with chronic skin inflammation developed albuminuria, histological evidence of glomerulosclerosis, and elevated blood pressure. KC-Tie2 mice had a selective and marked increase in circulating and renal neutrophils, along with increased neutrophil extracellular trap formation in the kidneys by flow cytometry. KC-Tie2 mice also exhibited increased bone marrow granulopoiesis along with increases in cutaneous and systemic G-CSF (granulocyte colony-stimulating factor), the primary mediator of granulopoiesis. Finally, neutralization of G-CSF decreased renal neutrophils and kidney damage in KC-Tie2 mice.
conclusionsOur findings demonstrate G-CSF-dependent increases in renal neutrophil accumulation and renal damage in a mouse model of psoriasis. Results suggest a novel link between chronic psoriasiform skin inflammation and renal damage via G-CSF-mediated granulopoiesis, providing new insight into interorgan communication in psoriasis and a potential new therapeutic target for the treatment of psoriasis-related renal dysfunction.
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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 Socratic graph.