ArticleProceedings of the National Academy of Sciences of the United States of America2020
Inhibition of 3-phosphoinositide-dependent protein kinase 1 (PDK1) can revert cellular senescence in human dermal fibroblasts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05854628 (The Role of Red Flavonoid in Photoaging), which is not on this map. Cited by 37 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
The Role of Red Flavonoid in Photoaging
Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
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- Phosphoinositide-dependent kinase 1 (PDK1) in cancer: molecular insights and therapeutic strategies.Frontiers in chemistry · 2026Review
- The relationship and predictive efficacy of serum lipocalin-2, PDK1, NGALR and lymph node metastasis in postmenopausal endometrial cancer.Translational cancer research · 2025Article
- Reverse control of biological networks to restore phenotype landscapes.Science advances · 2025Article
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Mechanotransduction for therapeutic approaches: Cellular aging and rejuvenation.APL bioengineering · 2025Review
- Senescent macrophages in cancer: roles in tumor progression and treatment opportunities.Cancer biology & medicine · 2025Review
- Senescence in the ageing skin: a new focus on mTORC1 and the lysosome.The FEBS journal · 2025Review
- Advances in biomarkers and diagnostic significance of organ aging.Fundamental research · 2025Review
- Dynamic 3D genome reorganization during senescence: defining cell states through chromatin.Cell death and differentiation · 2025Article
- Advances in the application of multi-omics analysis in skin aging.Frontiers in aging · 2025Review
- Atorvastatin calcium alleviates UVB-induced HaCat cell senescence and skin photoaging.Scientific reports · 2024Article
- Network dynamics-based subtyping of Alzheimer's disease with microglial genetic risk factors.Alzheimer's research & therapy · 2024Article
- Canalizing kernel for cell fate determination.Briefings in bioinformatics · 2024Article
- Combined inhibition of class 1-PI3K-alpha and delta isoforms causes senolysis by inducing p21Cell death & disease · 2024Article
- Novel Insights into Psychosis and Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes.International journal of molecular sciences · 2024Review
- Decoding the principle of cell-fate determination for its reverse control.NPJ systems biology and applications · 2024Article
- Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is defined as a stable, persistent arrest of cell proliferation. Here, we examine whether senescent cells can lose senescence hallmarks and reenter a reversible state of cell-cycle arrest (quiescence). We constructed a molecular regulatory network of cellular senescence based on previous experimental evidence. To infer the regulatory logic of the network, we performed phosphoprotein array experiments with normal human dermal fibroblasts and used the data to optimize the regulatory relationships between molecules with an evolutionary algorithm. From ensemble analysis of network models, we identified 3-phosphoinositide-dependent protein kinase 1 (PDK1) as a promising target for inhibitors to convert the senescent state to the quiescent state. We showed that inhibition of PDK1 in senescent human dermal fibroblasts eradicates senescence hallmarks and restores entry into the cell cycle by suppressing both nuclear factor κB and mTOR signaling, resulting in restored skin regeneration capacity. Our findings provide insight into a potential therapeutic strategy to treat age-related diseases associated with the accumulation of senescent cells.
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