ArticleAging cell2020
Activation of epidermal growth factor receptor signaling mediates cellular senescence induced by certain pro-inflammatory cytokines.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types.Aging cell · 2026Article
- Proteomic aging clocks in epidemiological studies: advances, applications and prospects.Nature aging · 2026Review
- Single-cell RNA sequencing reveals HMGA2 involvement in neoplastic aggressiveness and endothelial cell senescence in chondrosarcoma.Cell biology and toxicology · 2026Article
- LINC01996 suppresses non-small cell lung cancer proliferation and metastasis by orchestrating the miR-12115/CNRIP1/Ras signaling axis.Clinical & experimental metastasis · 2026Article
- A full-length single nuclei transcriptomic atlas of human skeletal muscle insulin resistance.bioRxiv : the preprint server for biology · 2026Article
- Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types.bioRxiv : the preprint server for biology · 2026Article
- Plasma proteomics identify novel biomarkers and dynamic patterns of biological aging.Journal of advanced research · 2026Article
- Inhibition of FXIIa attenuates kidney fibrosis in mice with unilateral ureteral obstruction.Cellular and molecular life sciences : CMLS · 2025Article
- The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.Molecular cancer · 2025Review
- Article
- Hyptolide Promotes Breast Cancer Stem Cells Apoptosis and S-phase Cell Cycle Arrest.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Healthy Aging Metabolomic and Proteomic Signatures Across Multiple Physiological Compartments.Aging cell · 2025Article
- NK cells: shielding senescence homeostasis in the decidua during early pregnancy.Seminars in immunopathology · 2025Review
- Impact of chitosan oligosaccharide on microbiota-metabolite-immune axis in natural aging.Frontiers in nutrition · 2025Article
- Review
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- Combined lineage tracing and scRNA-seq reveal the activation of Sox9Cell proliferation · 2024Article
- The Role of NRF2 in Cerebrovascular Protection: Implications for Vascular Cognitive Impairment and Dementia (VCID).International journal of molecular sciences · 2024Review
- Molecular Determinants of Neurocognitive Deficits in Glioma: Based on 2021 WHO Classification.Journal of molecular neuroscience : MN · 2024Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that inflammation in the body promotes organism aging, and recent studies have attributed a similar effect to senescent cells. Considering that certain pro-inflammatory cytokines can induce cellular senescence, systematically evaluating the effects of pro-inflammatory cytokines in cellular senescence is an important and urgent scientific problem, especially given the ongoing surge in aging human populations. Treating IMR90 cells and HUVECs with pro-inflammatory cytokines identified six factors able to efficiently induce cellular senescence. Of these senescence-inducing cytokines, the activity of five (namely IL-1β, IL-13, MCP-2, MIP-3α, and SDF-1α) was significantly inhibited by treatment with cetuximab (an antibody targeting epidermal growth factor receptor [EGFR]), gefitinib (a small molecule inhibitor of EGFR), and EGFR knockdown. In addition, treatment with one of the senescence-inducing cytokines, SDF-1α, significantly increased the phosphorylation levels of EGFR, as well as Erk1/2. These results suggested that pro-inflammatory cytokines induce cellular senescence by activating EGFR signaling. Next, we found that EGF treatment could also induce cellular senescence of IMR90 cells and HUVECs. Mechanically, EGF induced cellular senescence via excessive activation of Ras and the Ras-BRaf-Erk1/2 signaling axis. Moreover, EGFR activation induced IMR90 cells to secrete certain senescence-associated secretory phenotype factors (IL-8 and MMP-3). In summary, we report that certain pro-inflammatory cytokines induce cellular senescence through activation of the EGFR-Ras signaling pathway. Our study thus offers new insight into a long-ignored mechanism by which EGFR could regulate cellular senescence and suggests that growth signals themselves may catalyze aging under certain conditions.
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