ArticlePLoS computational biology2017
A model of the onset of the senescence associated secretory phenotype after DNA damage induced senescence.
Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
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- Data-driven inference of Boolean networks from transcriptomes to predict cellular differentiation and reprogramming.NPJ systems biology and applications · 2025Article
- Unveiling aging heterogeneities in human dermal fibroblasts via nanosensor chemical cytometry.Nature communications · 2025Article
- Mapping the attractor landscape of Boolean networks with biobalm.Bioinformatics (Oxford, England) · 2025Article
- Longevity cosmeceuticals as the next frontier in cosmetic innovation: a scientific framework for substantiating product claims.Frontiers in aging · 2025Review
- Boolean network modeling and its integration with experimental read-outs : An interdisciplinary presentation using a leukemia model.Pathologie (Heidelberg, Germany) · 2024Review
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- HHIP's Dynamic Role in Epithelial Wound Healing Reveals a Potential Mechanism of COPD Susceptibility.bioRxiv : the preprint server for biology · 2024Article
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- Xylosyltransferase-Deficiency in Human Dermal Fibroblasts Induces Compensatory Myofibroblast Differentiation and Long-Term ECM Reduction.Biomedicines · 2024Article
- Cellular senescence and wound healing in aged and diabetic skin.Frontiers in physiology · 2024Review
- Regulation of cellular senescence by innate immunity.Biophysics reports · 2023Article
- [Skin aging-cellular senescence : What is the future?]Dermatologie (Heidelberg, Germany) · 2023Review
- A systems biology approach to define mechanisms, phenotypes, and drivers in PanNETs with a personalized perspective.NPJ systems biology and applications · 2023Article
- Fibroblast heterogeneity: Keystone of tissue homeostasis and pathology in inflammation and ageing.Frontiers in immunology · 2023Review
- Ebselen, Iron Uptake Inhibitor, Alleviates Iron Overload-Induced Senescence-Like Neuronal Cells SH-SY5Y via Suppressing the mTORC1 Signaling Pathway.Advances in pharmacological and pharmaceutical sciences · 2023Article
- Immunomodulatory Nanosystems: Advanced Delivery Tools for Treating Chronic Wounds.Research (Washington, D.C.) · 2023Review
- Gut Microbiota and Aging: Traditional Chinese Medicine and Modern Medicine.Clinical interventions in aging · 2023Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells and tissues are exposed to stress from numerous sources. Senescence is a protective mechanism that prevents malignant tissue changes and constitutes a fundamental mechanism of aging. It can be accompanied by a senescence associated secretory phenotype (SASP) that causes chronic inflammation. We present a Boolean network model-based gene regulatory network of the SASP, incorporating published gene interaction data. The simulation results describe current biological knowledge. The model predicts different in-silico knockouts that prevent key SASP-mediators, IL-6 and IL-8, from getting activated upon DNA damage. The NF-κB Essential Modulator (NEMO) was the most promising in-silico knockout candidate and we were able to show its importance in the inhibition of IL-6 and IL-8 following DNA-damage in murine dermal fibroblasts in-vitro. We strengthen the speculated regulator function of the NF-κB signaling pathway in the onset and maintenance of the SASP using in-silico and in-vitro approaches. We were able to mechanistically show, that DNA damage mediated SASP triggering of IL-6 and IL-8 is mainly relayed through NF-κB, giving access to possible therapy targets for SASP-accompanied 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 OpenQuestion graph.