ArticleThe Journal of clinical investigation2022
Siglec-F-expressing neutrophils are essential for creating a profibrotic microenvironment in renal fibrosis.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 45 citations in OpenAlex.
- Disease-associated myeloid states in cardiac remodeling: A new era of cardiac inflammation research enabled by computational biology.The journal of physiological sciences : JPS · 2026Review
- Review
- A skin-kidney neutrophil axis links ultraviolet exposure to renal angiogenesis and tissue remodeling in healthy and lupus kidneys.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- SiglecF-expressing neutrophils differentiate from mature neutrophils locally in the heart after myocardial infarction.Experimental hematology · 2026Article
- Loss of erythrocyte sialic acid in sepsis disrupts inhibitory Siglec interactions, driving neutrophil hyperactivation and NET outspread.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Stem cell therapies to modulate harmful immune responses in kidney disease: progress toward clinical validation.Stem cells (Dayton, Ohio) · 2026Review
- Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Epithelial NLRP3 drives silica-induced lung injury and fibrosis through IL-18 and pro-fibrotic neutrophil recruitment.Particle and fibre toxicology · 2026Article
- A CD138+ tumor-associated macrophage/Siglec-F+ neutrophil feed-forward loop promotes immune evasion in pancreatic cancer.The Journal of clinical investigation · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation.Signal transduction and targeted therapy · 2026Article
- Structural immunity: immune cells as architects of tissue barriers.Nature reviews. Immunology · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Emerging therapeutic pipelines on kidney fibrosis: challenges in translational research.Journal of translational medicine · 2026Review
- Renal fibrosis: research progress on mechanisms and therapeutic strategies.Kidney research and clinical practice · 2026Article
- Immune cell fibrotic plasticity: mesenchymal-like reprogramming of macrophages, neutrophils and T cells.Frontiers in immunology · 2026Review
- Alterations in T lymphocyte subsets and mitochondrial-related parameters in patients with chronic kidney disease.Frontiers in medicine · 2026Article
- TGF-β in chronic kidney disease: a controversy for decades.Frontiers in immunology · 2026Review
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 2026Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The roles of neutrophils in renal inflammation are currently unclear. On examining these cells in the unilateral ureteral obstruction murine model of chronic kidney disease, we found that the injured kidney bore a large and rapidly expanding population of neutrophils that expressed the eosinophil marker Siglec-F. We first verified that these cells were neutrophils. Siglec-F+ neutrophils were recently detected in several studies in other disease contexts. We then showed that a) these cells were derived from conventional neutrophils in the renal vasculature by TGF-β1 and GM-CSF; b) they differed from their parent cells by more frequent hypersegmentation, higher expression of profibrotic inflammatory cytokines, and notably, expression of collagen 1; and c) their depletion reduced collagen deposition and disease progression, but adoptive transfer increased renal fibrosis. These findings have thus unveiled a subtype of neutrophils that participate in renal fibrosis and a potentially new therapeutic target in chronic kidney disease.
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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.