ArticleThe Journal of biological chemistry2013
Redox control of the senescence regulator interleukin-1α and the secretory phenotype.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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.
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Who cites it
45 citing papers in PubMed, 69 citations in OpenAlex.
- The senescence-inhibitory p53 isoform Δ133p53α represses the proinflammatory chemokine CXCL10 in progeria model mice and naturally aged mice.Geromedicine · 2026Article
- The states of senescent cells.Biochemical Society transactions · 2025Review
- The senescence-associated secretory phenotype and its physiological and pathological implications.Nature reviews. Molecular cell biology · 2024Review
- The Role of Intracellular Potassium in Cell Quiescence, Proliferation, and Death.International journal of molecular sciences · 2024Review
- Mitochondrial DNA is a key driver in cigarette smoke extract-induced IL-6 expression.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Therapy-induced senescence in breast cancer: an overview.Exploration of targeted anti-tumor therapy · 2024Review
- Salivary Gland Bioengineering.Bioengineering (Basel, Switzerland) · 2023Review
- Dynamics of redox signaling in aging via autophagy, inflammation, and senescence.Biogerontology · 2023Review
- 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
- Hallmarks and Biomarkers of Skin Senescence: An Updated Review of Skin Senotherapeutics.Antioxidants (Basel, Switzerland) · 2023Review
- Selenoproteins and the senescence-associated epitranscriptome.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- Expression of the Calcium-Binding Protein CALB1 Is Induced and Controls Intracellular CaInternational journal of molecular sciences · 2022Article
- Monovalent ions and stress-induced senescence in human mesenchymal endometrial stem/stromal cells.Scientific reports · 2022Article
- Radiobiological effects of wound fluid on breast cancer cell lines and human-derived tumor spheroids in 2D and microfluidic culture.Scientific reports · 2022Article
- Application of single and cooperative different delivery systems for the treatment of intervertebral disc degeneration.Frontiers in bioengineering and biotechnology · 2022Review
- A Comprehensive Overview of the Complex Role of Oxidative Stress in Aging, The Contributing Environmental Stressors and Emerging Antioxidant Therapeutic Interventions.Frontiers in aging neuroscience · 2022Review
- Review
- ROCK inhibition modulates the senescence-associated secretory phenotype (SASP) in oral keratinocytes.FEBS open bio · 2020Article
- Redox and mTOR-dependent regulation of plasma lamellar calcium influx controls the senescence-associated secretory phenotype.Experimental biology and medicine (Maywood, N.J.) · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Senescent cells accumulate in aged tissue and are causally linked to age-associated tissue degeneration. These non-dividing, metabolically active cells are highly secretory and alter tissue homeostasis, creating an environment conducive to metastatic disease progression. IL-1α is a key senescence-associated (SA) proinflammatory cytokine that acts as a critical upstream regulator of the SA secretory phenotype (SASP). We established that SA shifts in steady-state H2O2 and intracellular Ca(2+) levels caused an increase in IL-1α expression and processing. The increase in intracellular Ca(2+) promoted calpain activation and increased the proteolytic cleavage of IL-1α. Antioxidants and low oxygen tension prevented SA IL-1α expression and restricted expression of SASP components IL-6 and IL-8. Ca(2+) chelation or calpain inhibition prevented SA processing of IL-1α and its ability to induce downstream cytokine expression. Conditioned medium from senescent cells treated with antioxidants or Ca(2+) chelators or cultured in low oxygen markedly reduced the invasive capacity of proximal metastatic cancer cells. In this paracrine fashion, senescent cells promoted invasion by inducing an epithelial-mesenchymal transition, actin reorganization, and cellular polarization of neighboring cancer cells. Collectively, these findings demonstrate how SA alterations in the redox state and Ca(2+) homeostasis modulate the inflammatory phenotype through the regulation of the SASP initiator IL-1α, creating a microenvironment permissive to tumor invasion.
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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.