Musculoskeletal senescence: a moving target ready to be eliminated
Open accessAbstract
Aging is the prime risk factor for the broad-based development of diseases. Frailty is a phenotypical hallmark of aging and is often used to assess whether the predicted benefits of a therapy outweigh the risks for older patients. Senescent cells form as a consequence of unresolved molecular damage and persistently secrete molecules that can impair tissue function. Recent evidence shows senescent cells can chronically interfere with stem cell function and drive aging of the musculoskeletal system. In addition, targeted apoptosis of senescent cells can restore tissue homeostasis in aged animals. Thus, targeting cellular senescence provides new therapeutic opportunities for the intervention of frailty-associated pathologies and could have pleiotropic health benefits.
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Satellite cells are vulnerable to senescence, directly influencing their regenerative potential.
“Sousa-Victor and colleagues provided intriguing evidence that satellite cells are vulnerable to senescence, directly influencing their regenerative potential”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Baar et al., 2018
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Cellular senescence and aging in bone
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Biological Aging and Uterine Fibrosis in Cattle: Reproductive Trade-Offs from Enhanced Productivity
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Aging of the Musculoskeletal System
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Sarcopenia and the inflammatory cytokines
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Gene Expression Dynamics Underlying Muscle Aging in the Hawk Moth Manduca sexta
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Cell-type resolved transcriptional network analysis of in vivo cellular senescence following injury
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Modulating senescence for therapeutic delivery
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- Authors
- Baar, M. P., Perdiguero, E., Muñoz-Cánoves, P., & de Keizer, P. L.
- Affiliations
- Utrecht University (NL)
- Universitat Pompeu Fabra (ES)
- ORCID
- Perdiguero, Eusebio
- Venue
- Current Opinion in Pharmacology
- Publisher
- Elsevier BV
- Published
- 2018-06
- Volume
- 40
- Pages
- 147-155
- ISSN
- 1471-4892 (ISSN-L)
- OpenAlex
- W2807039864
- Cited by
- 83
- References
- 85
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 7 · 2023: 6 · 2022: 9 · 2021: 18 · 2020: 22 · 2019: 6
- FWCI
- 1.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Current Opinion in Pharmacology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion, other-oa)
- RECERCAT (Consorci de Serveis Universitaris de Catalunya) (publishedVersion, other-oa)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion, other-oa)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-sa)
- Repositori digital de la UPF (Universitat Pompeu Fabra) (submittedVersion, cc-by)
- Funders
- Dutch Cancer Society (UMCU-7141)
- 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 › Genetics › Mesenchymal stem cell research
- Keywords
- cellular senescence, musculoskeletal aging, frailty, senolytics, stem cell function, tissue homeostasis, senescence-associated secretory phenotype
- MeSH terms
- Age Factors, Animals, Bone and Bones, Cartilage, Humans, Musculoskeletal Diseases, Musculoskeletal System, Regeneration, Drug Design, Signal Transduction, Bone Remodeling, Cellular Senescence, Apoptosis, Muscle, Skeletal, Chondrogenesis, Muscle Development, Molecular Targeted Therapy
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