The YAP-TEAD complex promotes senescent cell survival by lowering endoplasmic reticulum stress
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Abstract
Sublethal cell damage can trigger senescence, a complex adaptive program characterized by growth arrest, resistance to apoptosis and a senescence-associated secretory phenotype (SASP). Here, a whole-genome CRISPR knockout screen revealed that proteins in the YAP-TEAD pathway influenced senescent cell viability. Accordingly, treating senescent cells with a drug that inhibited this pathway, verteporfin (VPF), selectively triggered apoptotic cell death largely by derepressing DDIT4, which in turn inhibited mTOR. Reducing mTOR function in senescent cells diminished endoplasmic reticulum (ER) biogenesis, triggering ER stress and apoptosis due to high demands on ER function by the SASP. Importantly, VPF treatment decreased the numbers of senescent cells in the organs of old mice and mice exhibiting doxorubicin-induced senescence. Moreover, VPF treatment reduced immune cell infiltration and pro-fibrotic transforming growth factor-β signaling in aging mouse lungs, improving tissue homeostasis. We present an alternative senolytic strategy that eliminates senescent cells by hindering ER activity required for SASP production.
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The TGFβ pathway representation in non-senescent epithelial cells from old lungs is consistent with enhanced paracrine signaling from increased numbers of senescent neighbors and with established features of epithelial aging.
“consistent with enhanced paracrine signaling from increased numbers of senescent neighbors and with established features of epithelial aging.23,25,32–35”
From SenCat: Cataloging human cell senescence through multi-omic profiling of multiple senescent primary cell types (2026) · cites this paper as [23]
In Results (‘VPF treatment reduces senescent cell burden in mice’; page unavailable), the paper reports age-associated TGF-β signatures in some lung epithelial cell types and TGF-β signaling from fibroblasts and capillary aerocytes affecting neighboring epithelial cells. This supports the proposed paracrine interpretation, but the paper does not establish that the epithelial cells are non-senescent or that increased numbers of senescent neighbors caused their pathway representation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredReliably detecting senescent cells within tissues and organs has been a central difficulty for the field.
“A major challenge in the field has been to reliably identify senescent cells in tissues and organs.23,25,32–35”
From SenCat: Cataloging human cell senescence through multi-omic profiling of multiple senescent primary cell types (2026) · cites this paper as [23]
The study required minimal or no cell death in senescence models to avoid noise from other damage responses such as apoptosis.
“we set the strict requirement that minimal or no cell death was seen to avoid noise from other forms of damage response such as apoptosis.21–23”
From SenCat: Cataloging human cell senescence through multi-omic profiling of multiple senescent primary cell types (2026) · cites this paper as [23]
The Methods section on cell culture and senescence induction describes the models and how cell viability was measured, but states no requirement for minimal or absent cell death. I searched for a cell-death threshold and for avoiding apoptosis as a confounding response; neither rationale appears in the retrieved passages (page numbers unavailable). (LLM, conf=0.74)
Experimental — accuracy not yet measured
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“This vulnerability is further highlighted by a CRISPR screen that identified how signalling through the transcription factor axis YAP–TEAD is needed to maintain the viability of SnCs 117 .”
Current senolytics: Mode of action, efficacy and limitations, and their future
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Oxidative stress and cellular senescence: Roles in tumor progression and therapeutic opportunities
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“Doxorubicin-induced senescence was triggered in 3-month-old C57BL/6 mice after a single dose of doxorubicin (10 mg per kg body weight); 10 days later, the mice were treated with DMSO or ABT-737 (50 mg per kg body weight) 28 .”
Self-citationEnhancing immunity during ageing by targeting interactions within the tissue environment
Bracken, O. V., Maeyer, R. P. H. D., & Akbar, A. N. (2025) · Nature Reviews Drug Discovery · doi:10.1038/s41573-024-01126-9 · Cited by 40 · see citing works
“Additionally, studies have shown that mTOR inhibition results in the death of senescent cells 166,167 .”
Central role of the ER proteostasis network in healthy aging
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Single-nucleus transcriptomics uncovers a geroprotective role of YAP in primate gingival aging
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“In contrast, YAP was also reported to accelerate vascular senescence (Pan et al., 2021) and promote the survival of senescent cells (Anerillas et al., 2023), consistent with a multi-faceted and context-dependent role for YAP signaling.”
BackgroundAnti-senescence therapies: a new concept to address cardiovascular disease
Stojanović, S. D., Thum, T., & Bauersachs, J. K. (2025) · Cardiovascular Research · doi:10.1093/cvr/cvaf030 · Cited by 28 · see citing works
“53 Senescent cells also evade death through resistance to scavenging and removal by immune cells.”
Genetic origins, regulators, and biomarkers of cellular senescence
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The Hippo signalling pathway in bone homeostasis: Under the regulation of mechanics and aging
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“5,6 Such modulations are linked to the development of aging-related conditions, including osteoarthritis and osteoporosis.”
BackgroundTRIM15 drives chondrocyte senescence and osteoarthritis progression
Li, Z., Zhang, W., Xiao, W., Hu, J. Z., Hu, X., Liu, H., Lü, J., Shen, S., & Ji, M.-L. (2025) · Science Translational Medicine · doi:10.1126/scitranslmed.adq1735 · Cited by 23 · see citing works
Transformation of peptides to small molecules in medicinal chemistry: Challenges and opportunities
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Necrosis Links Neurodegeneration and Neuroinflammation in Neurodegenerative Disease
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“The suppression of the YAP-TEAD axis has been implicated in cell senescence and ER dysfunction [63–65 , 69].”
BackgroundSenescence in cancer: Hallmarks, paradoxes, and therapeutic promise
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Systematic transcriptomic analysis and temporal modelling of human fibroblast senescence
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The Hippo Signaling Pathway Manipulates Cellular Senescence
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“In the aged human diploid fibroblast cell line, WI-38, the expression of genes in the YAP-TEAD1/2 pathway, particularly TEAD2, was shown to play a role in the viability of senescent cells [42].”
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E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence
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Cellular senescence in age-related musculoskeletal diseases
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“These findings indicate that senescent cell heterogeneity 54–56 , increasingly recognized in the field, is a key determinant of senolysis resistance.”
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Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation
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“Importantly, these metabolic and stress-response pathways converge on transcriptional programs that are regulated by mTOR-dependent mechanisms and the TEAD1/AP-1 complex, maintaining the activation of the SASP (Wang et al. 2022; Anerillas et al. 2023).”
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“…senescent cells comprising a variety of cytokines such as pro-in fl ammatory cytokines, growth factors, chemokines, and matrix-remodeling enzymes, these secretions play a role in inducing adjacent cells like recruiting immune cells and altering the phenotypic differentiation of immune cells (73).”
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“Sublethally damaged cells exhibit slower growth rates, reduced reproductive capacity, and heightened susceptibility to death when exposed to additional stressors (Anerillas et al., 2023).”
The aging extracellular matrix as a missing link in senescent cell accumulation and persistence
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“Recently, YAP– TEAD pathway was revealed to influence senescent cell viability by a whole-genome CRISPR knockout screen technique [36].”
BackgroundUFMylation maintains YAP stability to promote vascular endothelial cell senescence
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“21 The main mechanism of ECs YAP in promoting atherosclerosis is that YAP translocation into the nucleus promotes ECs activation with an inflammatory phenotype.”
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Sprouty1 is a broad mediator of cellular senescence
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Self-citationER stress-induced YAP upregulation leads to chondrocyte phenotype loss in age-related osteoarthritis
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Metabolic landscape and rewiring in normal hematopoiesis, leukemia and aging
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“Verteporfin treatment also decreased senescent cell burden and improved tissue homeostasis in aging mice, highlighting an alternative senolytic strategy targeting ER activity required for SASP production (Anerillas et al., 2023).”
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“26 In both experimental animals and humans, senescent cell numbers surge in a variety of disease states, including IDD, over time.”
GOREA: Unbiased Interpretation of Functional Enrichment
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Elimination of docetaxel-induced senescence attenuates malignant progression in RB1-deficient CRPC
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“Similarly, Gorospe et al.., showed that the YAP-TEAD complex facilitated senescent cell survival by mitigating endoplasmic reticulum (ER) stress through sustained mTOR activity, which in turn enhanced SASP production and prevented apoptosis [42 ].”
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“27 We also found that the YAP agonist XMU-MP-1 could reduce the release of mtDNA, which is align with previous study.”
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Distinct roles of COPI proteins attenuated in cell senescence
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“Briefly, senescence was triggered by culturing cells in media containing 50 μ M etoposide for 10 days, which causes sublethal damage leading to the cessation of cell proliferation ( 21 ).”
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- Authors
- Anerillas, C., Mazan-Mamczarz, K., Herman, A. B., Munk, R., Lam, K.-W. G., Calvo-Rubio, M., Garrido, A., Tsitsipatis, D., Martindale, J. L., Altés, G., Rossi, M., Piao, Y., Fan, J., Cui, C.-Y., De, S., Abdelmohsen, K., de Cabo, R., & Gorospe, M.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Anerillas, Carlos
- Gorospe, Myriam
- ORCID
- Venue
- Nature Aging
- Published
- 2023-09-04
- Volume
- 3
- Issue
- 10
- Pages
- 1237-1250
- ISSN
- 2662-8465 (ISSN-L)
- PMC
- PMC11369890
- OpenAlex
- W4386438437
- Semantic Scholar
- 1f5ad91456c178252279909f3ab09c724a21cf2a
- Cited by
- 76
- References
- 78
- Citations by year
- 2026: 26 · 2025: 26 · 2024: 21 · 2023: 1 · 2022: 1
- FWCI
- 13.07
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Licence
- Locations
- Nature Aging (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- Research Square (acceptedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- CINECA IRIS Institutial Research Information System (University of Genoa) (submittedVersion)
- Funders
- National Institute on Aging Intramural Research Program, NIH
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, senolytics, verteporfin, endoplasmic reticulum stress, senescence-associated secretory phenotype, DDIT4, mTOR inhibition, apoptosis, aging, pulmonary fibrosis, doxorubicin-induced senescence, immune cell infiltration, TGF-beta signaling
- MeSH terms
- YAP-Signaling Proteins, TEA Domain Transcription Factors, Aging, Animals, Cell Survival, Signal Transduction, Cellular Senescence, Mice, TOR Serine-Threonine Kinases, Endoplasmic Reticulum Stress
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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