Abstract
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.
Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Age Factors
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Animals
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Apoptosis / drug effects
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Bone Remodeling / drug effects
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Bone and Bones / drug effects
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Bone and Bones / metabolism
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Bone and Bones / pathology
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Bone and Bones / physiopathology
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Cartilage / drug effects
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Cartilage / metabolism
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Cartilage / pathology
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Cartilage / physiopathology
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Cellular Senescence / drug effects*
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Chondrogenesis / drug effects
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Drug Design
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Humans
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Molecular Targeted Therapy / methods*
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Muscle Development / drug effects
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Muscle, Skeletal / drug effects
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Muscle, Skeletal / metabolism
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Muscle, Skeletal / pathology
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Muscle, Skeletal / physiopathology
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Musculoskeletal Diseases / drug therapy*
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Musculoskeletal Diseases / metabolism
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Musculoskeletal Diseases / pathology
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Musculoskeletal Diseases / physiopathology
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Musculoskeletal System / drug effects*
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Musculoskeletal System / metabolism
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Musculoskeletal System / pathology
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Musculoskeletal System / physiopathology
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Regeneration / drug effects*
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Signal Transduction / drug effects