ArticleRedox biology2013
Redox-control of the alarmin, Interleukin-1α.
Article in Redox biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 34 citations in OpenAlex.
- M1 Macrophages Are a Source of IL-1α: A Driver of Progesterone Metabolism and Myometrial Contraction.Cells · 2025Article
- Proximity labelling of pro-interleukin-1α reveals evolutionary conserved nuclear interactions.Nature communications · 2024Article
- Goji-Berry-Mediated Green Synthesis of Gold Nanoparticles and Their Promising Effect on Reducing Oxidative Stress and Inflammation in Experimental Hyperglycemia.Antioxidants (Basel, Switzerland) · 2023Article
- Selenoproteins and the senescence-associated epitranscriptome.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Interleukin-1α associates with the tumor suppressor p53 following DNA damage.Scientific reports · 2020Article
- Nuclear Alarmin Cytokines in Inflammation.Journal of immunology research · 2020Review
- Cytokines in Inflammatory Disease.International journal of molecular sciences · 2019Review
- Article
- Function and regulation of IL-1α in inflammatory diseases and cancer.Immunological reviews · 2018Review
- Redox control of senescence and age-related disease.Redox biology · 2017Review
- Mitochondria control store-operated CaThe EMBO journal · 2017Article
- Critical role of calpain in inflammation.Biomedical reports · 2016Article
- Interleukin 1α and the inflammatory process.Nature immunology · 2016Review
- Article
- Off to a good start and a promising future in communicating cutting edge developments in redox biology.Redox biology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The pro-inflammatory cytokine Interleukin-1α (IL-1α) has recently emerged as a susceptibility marker for a wide array of inflammatory diseases associated with oxidative stress including Alzheimer's, arthritis, atherosclerosis, diabetes and cancer. In the present study, we establish that expression and nuclear localization of IL-1α are redox-dependent. Shifts in steady-state H2O2 concentrations (SS-[H2O2]) resulting from enforced expression of manganese superoxide dismutase (SOD2) drive IL-1α mRNA and protein expression. The redox-dependent expression of IL-1α is accompanied by its increased nuclear localization. Both IL-1α expression and its nuclear residency are abrogated by catalase co-expression. Sub-lethal doses of H2O2 also cause IL-1α nuclear localization. Mutagenesis revealed IL-1α nuclear localization does not involve oxidation of cysteines within its N terminal domain. Inhibition of the processing enzyme calpain prevents IL-1α nuclear localization even in the presence of H2O2. H2O2 treatment caused extracellular Ca(2+) influx suggesting oxidants may influence calpain activity indirectly through extracellular Ca(2+) mobilization. Functionally, as a result of its nuclear activity, IL-1α overexpression promotes NF-kB activity, but also interacts with the histone acetyl transferase (HAT) p300. Together, these findings demonstrate a mechanism by which oxidants impact inflammation through IL-1α and suggest that antioxidant-based therapies may prove useful in limiting inflammatory disease progression.
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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 OpenQuestion graph.