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Updated: Feb 13, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
IGF Binding Protein-5 Induces Cell Senescence
Fumihiro Sanada1, Yoshiaki Taniyama1,2, Jun Muratsu1,2
1Department of Clinical Gene Therapy, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Abstract:
Cellular senescence is the complex process of deterioration that drives the aging of an organism, resulting in the progressive loss of organ function and eventually phenotypic aging. Senescent cells undergo irreversible growth arrest, usually by inducing telomere shortening. Alternatively, senescence may also occur prematurely in response to various stress stimuli, such as oxidative stress, DNA damage, or activated oncogenes. Recently, it has been shown that IGF binding protein-5 (IGFBP-5) with the induction of the tumor suppressor p53 is upregulated during cellular senescence. This mechanism mediates interleukin-6/gp130-induced premature senescence in human fibroblasts, irradiation-induced premature senescence in human endothelial cells (ECs), and replicative senescence in human ECs independent of insulin-like growth factor I (IGF-I) and IGF-II. Additionally, a link between IGFBP-5, hyper-coagulation, and inflammation, which occur with age, has been implicated. Thus, IGFBP-5 seems to play decisive roles in controlling cell senescence and cell inflammation. In this review, we describe the accumulating evidence for this role of IGFBP-5 including our new finding.
Insights
Insulin-like growth factor-binding protein-5 (IGFBP-5) drives cellular senescence and inflammation. This protein is upregulated during aging, impacting organ function and potentially linking to age-related hyper-coagulation.
Area of Science:
- Gerontology
- Cell Biology
- Molecular Biology
Background:
- Cellular senescence is a key driver of organismal aging and organ dysfunction.
- Senescence involves irreversible growth arrest, often triggered by telomere shortening or stress.
- Senescent cells are linked to age-related inflammation and hyper-coagulation.
Purpose of the Study:
- To review the role of Insulin-like Growth Factor-binding Protein-5 (IGFBP-5) in cellular senescence and inflammation.
- To highlight the upregulation of IGFBP-5 during senescence, mediated by the tumor suppressor p53.
- To explore the implications of IGFBP-5 in age-related conditions.
Main Methods:
- Review of existing literature on cellular senescence and IGFBP-5.
- Analysis of studies demonstrating IGFBP-5 upregulation in various senescence models.
- Examination of the link between IGFBP-5, inflammation, and coagulation.
Main Results:
- IGFBP-5 is upregulated during cellular senescence, induced by p53.
- This upregulation mediates premature senescence in fibroblasts and endothelial cells (ECs).
- IGFBP-5 is implicated in age-related inflammation and hyper-coagulation.
Conclusions:
- IGFBP-5 plays a critical role in regulating cellular senescence and inflammation.
- The protein's involvement in senescence is independent of IGF-I and IGF-II.
- IGFBP-5 represents a potential therapeutic target for age-related diseases.
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