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Short-term senolytic treatment: a paradigm to promote fracture repair during aging
Increased age is blamed for a wide range of bone physiological changes, and although the underlying mechanisms affecting the decreased capacity for fracture healing are not fully understood, they are clearly linked to changes at the cellular level. Recent evidence suggests potential roles of senesce...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society for Clinical Investigation
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9012278/ https://www.ncbi.nlm.nih.gov/pubmed/35426369 http://dx.doi.org/10.1172/JCI158871 |
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author | Beerman, Isabel Basisty, Nathan de Cabo, Rafael |
author_facet | Beerman, Isabel Basisty, Nathan de Cabo, Rafael |
author_sort | Beerman, Isabel |
collection | PubMed |
description | Increased age is blamed for a wide range of bone physiological changes, and although the underlying mechanisms affecting the decreased capacity for fracture healing are not fully understood, they are clearly linked to changes at the cellular level. Recent evidence suggests potential roles of senescent cells in response to most tissue injuries, including bone fractures. In this issue of the JCI, Liu, Zhang, and co-authors showed that a senolytic drug cocktail cleared senescent cells from the callus and improved bone fracture repair in aged mice. Understanding how senescent cells emerge at fracture sites and how their timely removal improves fracture healing should provide insights for effective therapeutic approaches in old age. |
format | Online Article Text |
id | pubmed-9012278 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | American Society for Clinical Investigation |
record_format | MEDLINE/PubMed |
spelling | pubmed-90122782022-04-18 Short-term senolytic treatment: a paradigm to promote fracture repair during aging Beerman, Isabel Basisty, Nathan de Cabo, Rafael J Clin Invest Commentary Increased age is blamed for a wide range of bone physiological changes, and although the underlying mechanisms affecting the decreased capacity for fracture healing are not fully understood, they are clearly linked to changes at the cellular level. Recent evidence suggests potential roles of senescent cells in response to most tissue injuries, including bone fractures. In this issue of the JCI, Liu, Zhang, and co-authors showed that a senolytic drug cocktail cleared senescent cells from the callus and improved bone fracture repair in aged mice. Understanding how senescent cells emerge at fracture sites and how their timely removal improves fracture healing should provide insights for effective therapeutic approaches in old age. American Society for Clinical Investigation 2022-04-15 2022-04-15 /pmc/articles/PMC9012278/ /pubmed/35426369 http://dx.doi.org/10.1172/JCI158871 Text en © 2022 Beerman et al. https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Commentary Beerman, Isabel Basisty, Nathan de Cabo, Rafael Short-term senolytic treatment: a paradigm to promote fracture repair during aging |
title | Short-term senolytic treatment: a paradigm to promote fracture repair during aging |
title_full | Short-term senolytic treatment: a paradigm to promote fracture repair during aging |
title_fullStr | Short-term senolytic treatment: a paradigm to promote fracture repair during aging |
title_full_unstemmed | Short-term senolytic treatment: a paradigm to promote fracture repair during aging |
title_short | Short-term senolytic treatment: a paradigm to promote fracture repair during aging |
title_sort | short-term senolytic treatment: a paradigm to promote fracture repair during aging |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9012278/ https://www.ncbi.nlm.nih.gov/pubmed/35426369 http://dx.doi.org/10.1172/JCI158871 |
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