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The MTJ is particularly vulnerable to injuries compared to muscle and tendon and becomes more injury prone with age. Despite its clinical importance, the mechanisms driving MTJ ageing and age-related functional deterioration remain poorly understood. In this study, young (3-month-old) and old (23-month-old) male mice were used to provide the first comprehensive three-dimensional characterisation of age-related structural and cellular changes at the mouse Achilles MTJ. This was achieved using the high-resolution imaging techniques, micro-computed tomography (\u00b5CT) and confocal microscopy. \u00b5CT analysis revealed a 27% reduction in muscle fibre diameter with age, accompanied by a trend toward increased MTJ surface area and a 19% reduction in pennation angle, which may indicate diminished force generation capacity. Confocal imaging showed a 49% reduction in endothelial cell volume (VWF-labelled) in the old mouse muscle-tendon unit, suggesting a loss of vascularity. In situ hybridisation demonstrated increased expression of senescence markers p16 and p21 in endothelial and MTJ-specific cells, with MTJ-specific cells showing the greatest accumulation of p16 and p21 (270% and 310% increases, respectively) with age, and immunofluorescence also showed increased expression of p21. These findings suggest that vascular and MTJ-specific cells are particularly susceptible to ageing and may collectively contribute to the age-related functional decline of the MTJ. Understanding these mechanisms may help to develop targeted therapeutic strategies to preserve or restore MTJ integrity and function in ageing populations.<\/jats:p>","DOI":"10.1007\/s10522-026-10428-x","type":"journal-article","created":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T16:28:51Z","timestamp":1775320131000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ageing-related structural and cellular alterations in the mouse muscle-tendon junction"],"prefix":"10.1007","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7051-3504","authenticated-orcid":false,"given":"Chavaunne T.","family":"Thorpe","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-1660-1405","authenticated-orcid":false,"given":"Nodoka","family":"Iwasaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,4]]},"reference":[{"issue":"7372","key":"10428_CR1","doi-asserted-by":"publisher","first-page":"232","DOI":"10.1038\/nature10600","volume":"479","author":"DJ Baker","year":"2011","unstructured":"Baker DJ et al (2011) Clearance of p16 Ink4a-positive senescent cells delays ageing-associated disorders. 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