ArticleCell reports2017
Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 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.
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Who cites it
123 citing papers in PubMed, 188 citations in OpenAlex.
- Tumor-derived CTHRC1 mediates ITGB3-dependent osteoclast differentiation to promote prostate cancer bone metastasis.Oncogene · 2026Article
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Article
- The aging extracellular matrix as a missing link in senescent cell accumulation and persistence.Nature aging · 2026Article
- Polyploid Giant Cancer Cells as a Senescence-Linked State in the Tumor Microenvironment.Cancers · 2026Review
- Integrin β3 Promotes Retinal Neovascularization via Endoplasmic Reticulum Stress-Mediated Endothelial Cell Senescence.Investigative ophthalmology & visual science · 2026Article
- Article
- Emerging role of ARHGAP29 in melanoma cell phenotype switching.Molecular oncology · 2026Article
- DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The double-edged sword of SASP in breast cancer: from tumor suppression to progression and therapy resistance.Frontiers in oncology · 2026Review
- Arterial origin-dependent susceptibility of vascular smooth muscle cells to prelamin A-induced senescence and rescue by umbilical artery-derived decellularized extracellular matrix.International journal of clinical and experimental pathology · 2026Article
- Mechanical Signaling: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- A phosphorylation switch in the Mediator MED15 controls cellular senescence and cognitive decline.Cell discovery · 2025Article
- Involvement of TGF-β, mTOR, and inflammatory mediators in aging alterations during myxomatous mitral valve disease in a canine model.GeroScience · 2025Review
- Age-Related Dysregulation of α5β1 and αvβ3 Integrin Activity Alters Contractile Properties of Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2025Article
- ITGA1, the alpha 1 subunit of integrin receptor, is a novel marker of drug-resistant senescent melanoma cells in vitro.Archives of toxicology · 2025Article
- Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease.Cell death & disease · 2025Article
- Mechanical effects in aging of the musculoskeletal system: Molecular signaling and spatial scale alterations.Journal of orthopaedic translation · 2025Review
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- AMP-activated protein kinase (AMPK) is essential for tendon homeostasis and prevents premature senescence and ectopic calcification.bioRxiv : the preprint server for biology · 2025Article
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is an important in vivo mechanism that prevents the propagation of damaged cells. However, the precise mechanisms regulating senescence are not well characterized. Here, we find that ITGB3 (integrin beta 3 or β3) is regulated by the Polycomb protein CBX7. β3 expression accelerates the onset of senescence in human primary fibroblasts by activating the transforming growth factor β (TGF-β) pathway in a cell-autonomous and non-cell-autonomous manner. β3 levels are dynamically increased during oncogene-induced senescence (OIS) through CBX7 Polycomb regulation, and downregulation of β3 levels overrides OIS and therapy-induced senescence (TIS), independently of its ligand-binding activity. Moreover, cilengitide, an αvβ3 antagonist, has the ability to block the senescence-associated secretory phenotype (SASP) without affecting proliferation. Finally, we show an increase in β3 levels in a subset of tissues during aging. Altogether, our data show that integrin β3 subunit is a marker and regulator of senescence.
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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.