ArticleFEBS open bio2020
Interleukin-36α as a potential biomarker for renal tubular damage induced by dietary phosphate load.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Dietary phosphate exposure-strategies to protect vulnerable population groups.Archives of toxicology · 2026Review
- Renal tubular calcium phosphate microcrystallopathy and age-related kidney function decline: The Aging Kidney Study.Clinical kidney journal · 2026Article
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- Bone mineral loss damages renal tubules in mice.Communications biology · 2026Article
- Calcium Phosphate-Induced Injury in Kidney Tubular Cells-Supersaturated Solution vs Preformed Crystals.Journal of biochemical and molecular toxicology · 2025Article
- Correlative light and electron microscopic observation of calcium phosphate particles in a mouse kidney formed under a high-phosphate diet.Scientific reports · 2023Article
- Calcium phosphate microcrystals in the renal tubular fluid accelerate chronic kidney disease progression.The Journal of clinical investigation · 2021Article
- Klotho and calciprotein particles as therapeutic targets against accelerated ageing.Clinical science (London, England : 1979) · 2021Review
- Development of a Kidney Calcification Inhibitor Employing Image-Based Profiling: A Proof-of-Concept Study.ACS pharmacology & translational science · 2020Article
- Interleukin-36 Cytokine/Receptor Signaling: A New Target for Tissue Fibrosis.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive intake of phosphate has been known to induce renal tubular damage and interstitial inflammation, leading to acute kidney injury or chronic kidney disease in rodents and humans. However, sensitive and early biomarkers for phosphate-induced kidney damage remain to be identified. Our previous RNA sequencing analysis of renal gene expression identified interleukin-36α (IL-36α) as a gene significantly upregulated by dietary phosphate load in mice. To determine the time course and dose dependency of renal IL-36α expression induced by dietary phosphate load, we placed mice with or without uninephrectomy on a diet containing either 0.35%, 1.0%, 1.5%, or 2.0% inorganic phosphate for 10 days, 4 weeks, or 8 weeks and evaluated renal expression of IL-36α and other markers of tubular damage and inflammation by quantitative RT-PCR, immunoblot analysis, and immunohistochemistry. We found that IL-36α expression was induced in distal convoluted tubules and correlated with phosphate excretion per nephron. The increase in IL-36α expression was simultaneous with but more robust in amplitude than the increase in tubular damage markers such as Osteopontin and neutrophil gelatinase-associated lipocalin, preceding the increase in expression of other inflammatory cytokines, including transforming growth factor-α, interleukin-1β, and transforming growth factor-β1. We conclude that IL-36α serves as a marker that reflects the degree of phosphate load excreted per nephron and of associated kidney damage.
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