2026-06-16T14:05:24Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/65802024-09-27T09:53:11Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Baar, Marjolein P.
author
Perdiguero, Eusebio
author
Munoz-Canoves, Pura
author
de Keizer, Peter L. J.
funder
Dutch Cancer Society (Holanda)
funder
Unión Europea. Comisión Europea
funder
Ministerio de Economía y Competitividad (España)
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
2018-11-05T11:58:22Z
2018-11-05T11:58:22Z
2018
Curr Opin Pharmacol. 2018; 40:147-155
10.1016/j.coph.2018.05.007
1471-4973
1471-4892
Current Opinion in Pharmacology
29883814
http://hdl.handle.net/20.500.12105/6580
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.
eng
MESENCHYMAL STEM-CELLS
SKELETAL-MUSCLE REGENERATION
MARROW STROMAL CELLS
CELLULAR SENESCENCE
SATELLITE CELLS
KNEE OSTEOARTHRITIS
ARTICULAR-CARTILAGE
PROGENITOR CELLS
DNA-DAMAGE
POSTTRAUMATIC OSTEOARTHRITIS
Musculoskeletal senescence: a moving target ready to be eliminated
journal article
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MusculoskeletalSenescenceMoving _2018.pdf
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47589
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MusculoskeletalSenescenceMoving _2018.pdf.txt