A BDNF-TrkB autocrine loop enhances senescent cell viability
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Abstract
Cellular senescence is characterized by cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory phenotype (SASP) whereby cells secrete pro-inflammatory and tissue-remodeling factors. Given that the SASP exacerbates age-associated pathologies, some aging interventions aim at selectively eliminating senescent cells. In this study, a drug library screen uncovered TrkB (NTRK2) inhibitors capable of triggering apoptosis of several senescent, but not proliferating, human cells. Senescent cells expressed high levels of TrkB, which supported senescent cell viability, and secreted the TrkB ligand BDNF. The reduced viability of senescent cells after ablating BDNF signaling suggested an autocrine function for TrkB and BDNF, which activated ERK5 and elevated BCL2L2 levels, favoring senescent cell survival. Treatment with TrkB inhibitors reduced the accumulation of senescent cells in aged mouse organs. We propose that the activation of TrkB by SASP factor BDNF promotes cell survival and could be exploited therapeutically to reduce the senescent-cell burden.
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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 [21]
The Results section (“MAPK-directed drug screen,” page unavailable) says the WI-38 and BJ senescence conditions were optimized to produce minimal cell death. It does not say this was a strict requirement across the study’s senescence models or that the purpose was to avoid noise from other damage responses such as apoptosis. (LLM, conf=0.86)
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Cytokines and Madness: A Unifying Hypothesis of Schizophrenia Involving Interleukin-22
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TrkB signaling promotes alveolar capillary angiogenesis following perinatal hyperoxic damage
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Sprouty1 is a broad mediator of cellular senescence
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Systematic transcriptomic analysis and temporal modelling of the senescent human fibroblastPreprint
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The Aging Brain and Epilepsy: Current Knowledge and Novel Therapeutic Targets
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- Authors
- Anerillas, C., Herman, A. B., Munk, R., Garrido, A., Lam, K.-W. G., Payea, M. J., Rossi, M., Tsitsipatis, D., Martindale, J. L., Piao, Y., Mazan-Mamczarz, K., 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 Communications
- Published
- 2022-10-20
- Volume
- 13
- Issue
- 1
- Pages
- 6228-6228
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9585019
- OpenAlex
- W4306882651
- Cited by
- 35
- References
- 68
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 10 · 2023: 8 · 2022: 2
- FWCI
- 4.80
- Type
- journal article
- Language
- en
- Update notices
- correction (2022-12-07)
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Research Square (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (-0001, STAT3)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- cellular senescence, brain-derived neurotrophic factor, TrkB, autocrine signaling, senescence-associated secretory phenotype, senolytics, ERK5, BCL2L2, apoptosis resistance, senescent cell elimination, aging
- MeSH terms
- Animals, Cell Survival, Humans, Ligands, Membrane Glycoproteins, Cellular Senescence, Apoptosis, Brain-Derived Neurotrophic Factor, Receptor, trkB, Mice
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