ArticleCell death & disease2013
Insulin-like growth factor binding proteins 4 and 7 released by senescent cells promote premature senescence in mesenchymal stem cells.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
135 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.
- Meta-analysis of senescent cell secretomes to identify common and specific features of the different senescent phenotypes: a tool for developing new senotherapeutics.Cell communication and signaling : CCS · 2023Pooled it
- Circulating IGFBP-7 in Obstructive Sleep Apnea: A Single-Cohort Preliminary Assessment of Its Diagnostic Performance and Post-Treatment Dynamics.Biomedicines · 2026Article
- Plasma insulin-like growth Factor-Binding protein 7 predicts 20-Year Cancer-Specific and overall survival in ARIC.Journal of the National Cancer Institute · 2026Article
- Circulating levels of insulin-like growth factor binding protein 7 are associated with risks of chronic diseases and death.npj aging · 2026Article
- Bidirectional Interactions Between Immune Regulation and the Insulin-like Growth Factor Axis in Colorectal Cancer.International journal of molecular sciences · 2026Review
- Tooth Decay Promotes Senescence in Dental Pulp Stem Cells, Modifying Their Biological and Proteomic Profiles.Journal of cellular physiology · 2026Article
- Endothelial Dysfunction Contributes to Chondrocyte Senescence Associated With Insulin-Like Growth Factor-Binding Protein-6 in a Spontaneously Hypertensive Rat Model.Journal of the American Heart Association · 2026Article
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- Balancing senescence and apoptosis: therapeutic insights into aging and cancer.Molecular and cellular biochemistry · 2025Review
- Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells.Molecular oncology · 2025Article
- Ontogenetic stage and type of donor cells shape extracellular vesicles' therapeutic potential for osteoarthritis.Stem cell research & therapy · 2025Article
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- Article
- Molecular Regulation of SASP in Cellular Senescence: Therapeutic Implications and Translational Challenges.Cells · 2025Review
- The IGF System and Aging.Endocrine reviews · 2025Review
- The role of GATA4 in mesenchymal stem cell senescence: A new frontier in regenerative medicine.Regenerative therapy · 2025Review
- Association between Insulin-Like Growth Factor Binding Protein-7 and Heart Failure.Current medicinal chemistry · 2025Review
- The senescence-inducing factor IGFBP7 and risk of atrial fibrillation: findings from the PREVEND study.NPJ cardiovascular health · 2025Article
- The impact of cellular senescence on aging skeletal muscle.Frontiers in cell and developmental biology · 2025Review
- Proteomic Alterations in Retinal Müller Glial Cells Lacking Interleukin-6 Receptor: A Comprehensive Analysis.Investigative ophthalmology & visual science · 2024Article
75 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is the permanent arrest of cell cycle, physiologically related to aging and aging-associated diseases. Senescence is also recognized as a mechanism for limiting the regenerative potential of stem cells and to protect cells from cancer development. The senescence program is realized through autocrine/paracrine pathways based on the activation of a peculiar senescence-associated secretory phenotype (SASP). We show here that conditioned media (CM) of senescent mesenchymal stem cells (MSCs) contain a set of secreted factors that are able to induce a full senescence response in young cells. To delineate a hallmark of stem cells SASP, we have characterized the factors secreted by senescent MSC identifying insulin-like growth factor binding proteins 4 and 7 (IGFBP4 and IGFBP7) as key components needed for triggering senescence in young MSC. The pro-senescent effects of IGFBP4 and IGFBP7 are reversed by single or simultaneous immunodepletion of either proteins from senescent-CM. The blocking of IGFBP4/7 also reduces apoptosis and promotes cell growth, suggesting that they may have a pleiotropic effect on MSC biology. Furthermore, the simultaneous addition of rIGFBP4/7 increased senescence and induced apoptosis in young MSC. Collectively, these results suggest the occurrence of novel-secreted factors regulating MSC cellular senescence of potential importance for regenerative medicine and cancer therapy.
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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.