ArticleClinical and experimental immunology2018
S100A8/A9 promotes parenchymal damage and renal fibrosis in obstructive nephropathy.
Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- S100A1 Promotes MDM2-Mediated KLF15 Ubiquitination to Regulate ID1-Driven Tubular Injury in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Genome-wide DNA methylation analysis revealed epigenetic mechanism underlying end-stage renal disease.Nature communications · 2026Article
- The Role of Neutrophil, Monocyte and Macrophage Calprotectin and S100A12 in the Fibrotic Process.Biomolecules · 2026Review
- S100A8/A9 in Kidney Diseases: Mechanisms, Spatiotemporal Regulation, Biomarker Potential, and Therapeutic Implications.Journal of inflammation research · 2026Review
- Urinary Calprotectin Predicts Severe Acute Kidney Injury After Non-cardiac Surgery in Surgical Intensive Care Unit: A Prospective Cohort Study.Biomarker insights · 2026Article
- Inhibition of FXIIa attenuates kidney fibrosis in mice with unilateral ureteral obstruction.Cellular and molecular life sciences : CMLS · 2025Article
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- Serum S100A8/A9 Correlates to Surgery-Free Interval in Idiopathic Subglottic Stenosis.The Laryngoscope · 2025Article
- Effects of Graphene Quantum Dots on Renal Fibrosis Through Alleviating Oxidative Stress and Restoring Mitochondrial Membrane Potential.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Discovery and serological validation of DAMP-derived B-cell epitopes as diagnostic biomarkers for diabetic nephropathy.Frontiers in endocrinology · 2025Article
- Single-cell RNA sequencing reveals that myeloid S100A8/A9 is a novel regulator of the transition from adaptive hypertrophy to heart failure after pressure overload.Theranostics · 2025Article
- S100A8/S100A9 through PAD4 activation of neutrophil extracellular traps promotes granulomatous lobular mastitis.Frontiers in immunology · 2025Article
- Neutrophil-secreted S100A8/A9 participates in fatty liver injury and fibrosis by promoting myofibroblast migration.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Article
- High S100A9 level predicts poor survival, and the S100A9 inhibitor paquinimod is a candidate for treating idiopathic pulmonary fibrosis.BMJ open respiratory research · 2024Article
- NLRX1 Prevents M2 Macrophage Polarization and Excessive Renal Fibrosis in Chronic Obstructive Nephropathy.Cells · 2023Article
- Prediction of acute kidney injury incidence following acute type A aortic dissection surgery with novel biomarkers: a prospective observational study.BMC medicine · 2023Observational
- The role of toll-like receptors (TLRs) and their therapeutic applications in glomerulonephritis.International urology and nephrology · 2023Review
- Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis.Physiological reviews · 2023Review
- Exercise training remodels inguinal white adipose tissue through adaptations in innervation, vascularization, and the extracellular matrix.Cell reports · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite advances in our understanding of the mechanisms underlying the progression of chronic kidney disease and the development of fibrosis, only limited efficacious therapies exist. The calcium binding protein S100A8/A9 is a damage-associated molecular pattern which can activate Toll-like receptor (TLR)-4 or receptor for advanced glycation end-products (RAGE). Activation of these receptors is involved in the progression of renal fibrosis; however, the role of S100A8/A9 herein remains unknown. Therefore, we analysed S100A8/A9 expression in patients and mice with obstructive nephropathy and subjected wild-type and S100A9 knock-out mice lacking the heterodimer S100A8/A9 to unilateral ureteral obstruction (UUO). We found profound S100A8/A9 expression in granulocytes that infiltrated human and murine kidney, together with enhanced renal expression over time, following UUO. S100A9 KO mice were protected from UUO-induced renal fibrosis, independently of leucocyte infiltration and inflammation. Loss of S100A8/A9 protected tubular epithelial cells from UUO-induced apoptosis and critical epithelial-mesenchymal transition steps. In-vitro studies revealed S100A8/A9 as a novel mediator of epithelial cell injury through loss of cell polarity, cell cycle arrest and subsequent cell death. In conclusion, we demonstrate that S100A8/A9 mediates renal damage and fibrosis, presumably through loss of tubular epithelial cell contacts and irreversible damage. Suppression of S100A8/A9 could be a therapeutic strategy to halt renal fibrosis in patients with 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.