Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature

Abstract The senescence-associated secretory phenotype (SASP) is a generic term for the secretion of cytokines, such as pro-inflammatory factors and proteases. It is a crucial feature of senescent cells. SASP factors induce tissue remodeling and immune cell recruitment. Previous studies have focused...

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Main Authors: Shangkun Zhao, Zhi Qiao, Roman Pfeifer, Hans-Christoph Pape, Keya Mao, Hai Tang, Bin Meng, Songfeng Chen, Hongjian Liu
Format: Article
Language:English
Published: BMC 2024-01-01
Series:European Journal of Medical Research
Subjects:
Online Access:https://doi.org/10.1186/s40001-023-01604-7
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author Shangkun Zhao
Zhi Qiao
Roman Pfeifer
Hans-Christoph Pape
Keya Mao
Hai Tang
Bin Meng
Songfeng Chen
Hongjian Liu
author_facet Shangkun Zhao
Zhi Qiao
Roman Pfeifer
Hans-Christoph Pape
Keya Mao
Hai Tang
Bin Meng
Songfeng Chen
Hongjian Liu
author_sort Shangkun Zhao
collection DOAJ
description Abstract The senescence-associated secretory phenotype (SASP) is a generic term for the secretion of cytokines, such as pro-inflammatory factors and proteases. It is a crucial feature of senescent cells. SASP factors induce tissue remodeling and immune cell recruitment. Previous studies have focused on the beneficial role of SASP during embryonic development, wound healing, tissue healing in general, immunoregulation properties, and cancer. However, some recent studies have identified several negative effects of SASP on fracture healing. Senolytics is a drug that selectively eliminates senescent cells. Senolytics can inhibit the function of senescent cells and SASP, which has been found to have positive effects on a variety of aging-related diseases. At the same time, recent data suggest that removing senescent cells may promote fracture healing. Here, we reviewed the latest research progress about SASP and illustrated the inflammatory response and the influence of SASP on fracture healing. This review aims to understand the role of SASP in fracture healing, aiming to provide an important clinical prevention and treatment strategy for fracture. Clinical trials of some senolytics agents are underway and are expected to clarify the effectiveness of their targeted therapy in the clinic in the future. Meanwhile, the adverse effects of this treatment method still need further study.
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spelling doaj.art-fa60692785ea4f38acd9bb35bb5966f72024-01-14T12:16:36ZengBMCEuropean Journal of Medical Research2047-783X2024-01-0129111210.1186/s40001-023-01604-7Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literatureShangkun Zhao0Zhi Qiao1Roman Pfeifer2Hans-Christoph Pape3Keya Mao4Hai Tang5Bin Meng6Songfeng Chen7Hongjian Liu8Department of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou UniversityDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou UniversityDepartment of Traumatology, University Hospital of ZurichDepartment of Traumatology, University Hospital of ZurichChinese PLA General Hospital BeijingBeijing Friendship HospitalFirst Affiliated Hospital of Soochow UniversityDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou UniversityDepartment of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou UniversityAbstract The senescence-associated secretory phenotype (SASP) is a generic term for the secretion of cytokines, such as pro-inflammatory factors and proteases. It is a crucial feature of senescent cells. SASP factors induce tissue remodeling and immune cell recruitment. Previous studies have focused on the beneficial role of SASP during embryonic development, wound healing, tissue healing in general, immunoregulation properties, and cancer. However, some recent studies have identified several negative effects of SASP on fracture healing. Senolytics is a drug that selectively eliminates senescent cells. Senolytics can inhibit the function of senescent cells and SASP, which has been found to have positive effects on a variety of aging-related diseases. At the same time, recent data suggest that removing senescent cells may promote fracture healing. Here, we reviewed the latest research progress about SASP and illustrated the inflammatory response and the influence of SASP on fracture healing. This review aims to understand the role of SASP in fracture healing, aiming to provide an important clinical prevention and treatment strategy for fracture. Clinical trials of some senolytics agents are underway and are expected to clarify the effectiveness of their targeted therapy in the clinic in the future. Meanwhile, the adverse effects of this treatment method still need further study.https://doi.org/10.1186/s40001-023-01604-7Fracture healingBoneSenescenceSASPSenolytics
spellingShingle Shangkun Zhao
Zhi Qiao
Roman Pfeifer
Hans-Christoph Pape
Keya Mao
Hai Tang
Bin Meng
Songfeng Chen
Hongjian Liu
Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature
European Journal of Medical Research
Fracture healing
Bone
Senescence
SASP
Senolytics
title Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature
title_full Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature
title_fullStr Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature
title_full_unstemmed Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature
title_short Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature
title_sort modulation of fracture healing by senescence associated secretory phenotype sasp a narrative review of the current literature
topic Fracture healing
Bone
Senescence
SASP
Senolytics
url https://doi.org/10.1186/s40001-023-01604-7
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