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Here, we combined single\u2010cell RNA\u2010seq with 2\u2010\u00b5m Visium HD spatial transcriptomics to define stage\u2010specific changes in\n                    <jats:italic>Prrx1<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    SuSCs in the\n                    <jats:italic>\n                      Fgfr2\n                      <jats:sup>C342Y\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mouse model. We observed early downregulation of\n                    <jats:italic>Frizzled\u20107<\/jats:italic>\n                    (\n                    <jats:italic>Fzd7<\/jats:italic>\n                    ), increased mitophagy\u2010associated signatures and readouts with elevated\n                    <jats:italic>Pink1<\/jats:italic>\n                    expression, and premature osteogenic activation within the SuSC niche. In vitro, loss of\n                    <jats:italic>Fzd7<\/jats:italic>\n                    increased mitophagy and osteogenic activity, whereas\n                    <jats:italic>Fzd7<\/jats:italic>\n                    overexpression attenuated these changes. In vivo, conditional deletion of\n                    <jats:italic>Fzd7<\/jats:italic>\n                    accelerated coronal suture fusion, while AAV\u2010mediated\n                    <jats:italic>Fzd7<\/jats:italic>\n                    overexpression reduced fusion. Conditional deletion of\n                    <jats:italic>Pink1<\/jats:italic>\n                    suppressed the effects of\n                    <jats:italic>Fzd7<\/jats:italic>\n                    loss, supporting\n                    <jats:italic>Pink1<\/jats:italic>\n                    \u2010dependent mitophagy as a required component of the\n                    <jats:italic>Fzd7<\/jats:italic>\n                    \u2010deficiency\u2010associated osteogenic and fusion phenotypes. These findings support a model in which an\n                    <jats:italic>Fzd7\u2013Pink1<\/jats:italic>\n                    mitophagy axis contributes to the maintenance of suture patency in craniosynostosis and provide a mechanistic basis for future targeted studies.\n                  <\/jats:p>","DOI":"10.1002\/advs.77245","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T13:47:31Z","timestamp":1787147251000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<i>Fzd7<\/i>\n                    Restrains\n                    <i>Pink1<\/i>\n                    \u2010Dependent Mitophagy in Suture Stem Cells to Maintain Cranial Suture Patency"],"prefix":"10.1002","author":[{"given":"Xinyan","family":"Chen","sequence":"first","affiliation":[{"name":"Craniomaxillofacial Surgery Department Plastic Surgery Hospital Chinese Academy of Medical Sciences &amp; Peking Union Medical 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