ArticleNature cell biology2023
COPI vesicle formation and N-myristoylation are targetable vulnerabilities of senescent cells.
Article in Nature cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 49 citations in OpenAlex.
- Senescence-directed nanotherapy ameliorates fibrosis and overcomes immune exclusion in cancer.Science (New York, N.Y.) · 2026Article
- Molecular mechanisms and pathogenesis of MASH.Nature · 2026Review
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- SenFlag gene signature identifies senescent cells in mouse and human tissues through a conserved core transcriptional program.The EMBO journal · 2026Article
- Distinct roles of COPI proteins attenuated in cell senescence.Science advances · 2026Article
- YIF1A activates mTORC1 signaling to promote cellular senescence.Cell death & disease · 2026Article
- Exploring molecular signatures of senescence with marker, an R Toolkit for evaluating gene sets as phenotypic markers.NAR genomics and bioinformatics · 2026Article
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Inhibition of host N-myristoylation compromises the infectivity of SARS-CoV-2 due to Golgi-bypassing egress.Nature communications · 2026Article
- Electrophilic compound screening identifies GPX4-dependent ferroptosis as a senescence vulnerability.Nature cell biology · 2026Article
- Review
- New payloads drive next-gen antibody-drug conjugates.Nature cancer · 2026Article
- Comparative analysis of senolytic drugs reveals mitochondrial determinants of efficacy and resistance.Nature aging · 2026Article
- Pharmacological Myristoylation Inhibition by Zelenirstat Disrupts Growth Signalling, Energy Metabolism, and Migration in Triple-Negative Breast Cancer Cells.Breast cancer (Dove Medical Press) · 2026Article
- The Microbial Metabolite IDA Sensitizes Tumor Cells to ARF1 Inhibition by Inducing SVIL-dependent Senescence.International journal of biological sciences · 2026Article
- Navitoclax acts synergistically with irradiation to induce apoptosis in preclinical models of H3K27M-altered diffuse midline glioma.Scientific reports · 2025Article
- Mitochondrial RNA cytosolic leakage drives the SASP.Nature communications · 2025Article
- The drug discovery and therapeutic nano-strategies targeting cellular senescence.Materials today. Bio · 2025Review
- Improving our understanding of the biology of aging: findings from the Age-It Research Program.The journals of gerontology. Series B, Psychological sciences and social sciences · 2025Article
- Directed rescue strategy for enhanced implant osteointegration in aged rats.Nature communications · 2025Article
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 4 countries.
Funding
Abstract
Drugs that selectively kill senescent cells (senolytics) improve the outcomes of cancer, fibrosis and age-related diseases. Despite their potential, our knowledge of the molecular pathways that affect the survival of senescent cells is limited. To discover senolytic targets, we performed RNAi screens and identified coatomer complex I (COPI) vesicle formation as a liability of senescent cells. Genetic or pharmacological inhibition of COPI results in Golgi dispersal, dysfunctional autophagy, and unfolded protein response-dependent apoptosis of senescent cells, and knockdown of COPI subunits improves the outcomes of cancer and fibrosis in mouse models. Drugs targeting COPI have poor pharmacological properties, but we find that N-myristoyltransferase inhibitors (NMTi) phenocopy COPI inhibition and are potent senolytics. NMTi selectively eliminated senescent cells and improved outcomes in models of cancer and non-alcoholic steatohepatitis. Our results suggest that senescent cells rely on a hyperactive secretory apparatus and that inhibiting trafficking kills senescent cells with the potential to treat various senescence-associated diseases.
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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 Socratic graph.