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Here, we identify Microtubule Actin Cross\u2010linking Factor 1 (MACF1) as a critical regulator of MSC fate that is severely suppressed during long\u2010term glucocorticoid (GC) exposure. We demonstrate that MACF1 deficiency phenocopies GC\u2010induced marrow adiposity and bone loss. Crucially, restoring endogenous MACF1 via promoter\u2010targeted small activating RNA (saRNA) effectively corrects this fate bias and reverses microarchitectural deterioration in GIO mice. Mechanistically, MACF1 acts as a key facilitator of vesicular trafficking. By orchestrating the assembly of the Rab14\/KIF16B complex, MACF1 drives the precise anterograde transport of Fibroblast Growth Factor Receptors (FGFRs) to the plasma membrane. GC exposure downregulates MACF1, disrupting this transport machinery and causing intracellular FGFR sequestration. This transport failure depletes functional cell\u2010surface FGFRs, thereby blunting osteogenic signaling and triggering the adipogenic shift. Collectively, our findings establish the MACF1\u2010governed intracellular trafficking network as an important determinant of FGFR spatial distribution and MSC fate, highlighting it as a promising therapeutic target for restoring bone\u2010fat equilibrium in GIO.<\/jats:p>","DOI":"10.1002\/advs.77073","type":"journal-article","created":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T14:32:29Z","timestamp":1786372349000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Dysregulation of the MACF1\u2010Rab14\/KIF16B\u2010FGFR Vesicular Trafficking Axis Skews MSC Lineage Commitment in Glucocorticoid\u2010Induced Osteoporosis"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3657-3129","authenticated-orcid":false,"given":"Peihong","family":"Su","sequence":"first","affiliation":[{"name":"Shaanxi Provincial Key Laboratory of Ischemic Cardiovascular Disease Institute of Basic and Translational 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