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Published on: June 28, 2019
Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments
Zhengdong Zhang1,2,3, Pan Liu4, Yu Song1
1Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background:
Osteoblast senescence is a central driverof age-related osteoporosis. Accumulating evidence shows that counteractingthis senescence can substantially mitigate bone loss. In this review, we summarize the hallmarks of osteoblast senescence, the signaling pathways involved, and therapeutic strategies that target osteoblast senescence tocombat age-related osteoporosis.
Methods:
Chronic diseases associated with ageingpose a significant threat to human health. Studies have shown that osteoporosisis closely linked to the ageing process of the body and the senescence ofosteoblasts within the bone microenvironment. Counteracting the senescence ofosteoblasts and maintaining the balance of differentiation, proliferation andfunction between osteoclasts and osteoblasts has been a key focus in the research of age-related osteoporosis and bone loss. The biological behaviour andfunctionality of the osteoblast lineage related to senescence are modulated bya variety of targets, including signalling pathways, proteins and genes associated with ageing. This review aims to discuss the senescence-related characteristics of the osteoblast lineage, dissect the interplay and mechanisms between it and ageing-associated signalling pathways, proteinsand genes, as well as current strategies for the prevention and treatment ofosteoblast senescence.
Conclusion:
This review systematically examines the regulatory interactions among markers, therapeutic targets, and signalingpathways associated with osteoblast senescence, alongside current potential strategies for targeting this process. It provides more comprehensive information for future research into the complex mechanisms underlying age-related osteoporosis driven by osteoblast senescence.
Key Points:
Osteoblast senescence is a key driver of age-related osteoporosis, disrupting bone formation and homeostasis. Aging impacts osteoblasts through multiple pathways, including telomere shortening, genomic instability, SASP secretion, and others. Bone loss related to osteoblast senescence involves the activation and crosstalk of multiple signaling pathways. The options for combating and treating osteoblast senescence toachieve anti-osteoporosis are numerous, but still challenging.
Insights
Osteoblast senescence drives age-related osteoporosis by disrupting bone formation. Counteracting this process offers therapeutic potential for mitigating bone loss and treating osteoporosis.
Area of Science:
- Gerontology
- Cell Biology
- Bone Biology
Background:
- Osteoblast senescence is a primary contributor to age-related osteoporosis.
- Counteracting osteoblast senescence can significantly reduce bone loss.
- Understanding these mechanisms is crucial for developing effective osteoporosis treatments.
Purpose of the Study:
- To review the hallmarks of osteoblast senescence.
- To explore the signaling pathways involved in osteoblast senescence.
- To summarize therapeutic strategies targeting osteoblast senescence for age-related osteoporosis.
Main Methods:
- Review of current literature on osteoblast senescence and osteoporosis.
- Analysis of signaling pathways, proteins, and genes modulating osteoblast senescence.
- Examination of therapeutic strategies for preventing and treating osteoblast senescence.
Main Results:
- Osteoblast senescence disrupts bone formation and homeostasis through pathways like telomere shortening and SASP secretion.
- Age-related bone loss involves complex signaling pathway crosstalk.
- Multiple therapeutic targets exist, but challenges remain in treatment.
Conclusions:
- Osteoblast senescence is a critical factor in age-related osteoporosis.
- Targeting osteoblast senescence presents promising therapeutic avenues.
- Further research is needed to fully elucidate mechanisms and optimize treatments.
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