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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\u2010related osteoporosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>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\u2010related 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\u2010related characteristics of the osteoblast lineage, dissect the interplay and mechanisms between it and ageing\u2010associated signalling pathways, proteinsand genes, as well as current strategies for the prevention and treatment ofosteoblast senescence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>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\u2010related osteoporosis driven by osteoblast senescence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Osteoblast senescence is a key driver of age\u2010related osteoporosis, disrupting bone formation and homeostasis.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Aging impacts osteoblasts through multiple pathways, including telomere shortening, genomic instability, SASP secretion, and others.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Bone loss related to osteoblast senescence involves the activation and crosstalk of multiple signaling pathways.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The options for combating and treating osteoblast senescence toachieve anti\u2010osteoporosis are numerous, but still challenging.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/ctm2.70417","type":"journal-article","created":{"date-parts":[[2025,7,19]],"date-time":"2025-07-19T02:29:13Z","timestamp":1752892153000},"source":"Crossref","is-referenced-by-count":16,"title":["Addressing osteoblast senescence: Molecular pathways and the frontier of anti\u2010ageing treatments"],"prefix":"10.1002","volume":"15","author":[{"given":"Zhengdong","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Orthopaedics Union Hospital Tongji Medical College Huazhong University of Science and Technology  Wuhan China"},{"name":"School of Clinical Medicine Chengdu Medical College  Chengdu China"},{"name":"Department of Orthopaedics The First Affiliated Hospital of Chengdu Medical College  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pan","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Endocrinology Hospital 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