ArticleGlycobiology2026
Comprehensive analysis of the skeletal phenotype in Chst14-/- mice: implications for dermatan sulfate in bone structure and strength.
Article in Glycobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Dermatan sulfate (DS) is a glycosaminoglycan known to contribute to tissue strength through collagen fibril assembly. Musculocontractural Ehlers-Danlos syndrome (mcEDS) caused by pathogenic variants in the gene that encodes carbohydrate sulfotransferase 14 (CHST14) (mcEDS-CHST14) is a representative disorder of DS deficiency. Skeletal lesions, such as progressive spinal deformity and osteoporosis/osteopenia, are significant manifestations of mcEDS-CHST14, which can lead to deterioration in quality of life. To characterize skeletal alterations associated with DS deficiency, we performed comprehensive analyses of the skeletal phenotypes in Chst14 gene-deleted (Chst14-/-) mice. Chst14-/- mice exhibited progressive kyphosis, proximal femoral deformities, and decreased bone strength, as well as reduced trabecular bone mass and structural parameters, from a young age. Qualitative ultrastructural alterations of collagen fibrils in cortical bone were observed in middle-aged Chst14-/- mice by transmission electron microscopy. In addition, cortical bone showed increased expression of receptor activator of NF-κB (Rank), a gene involved in osteoclast differentiation, in middle age. Histomorphometric analyses of cancellous bone demonstrated reduced trabecular structural parameters in Chst14-/- mice, including decreases in bone volume and trabecular number. These findings indicate age-dependent alterations in both cortical and cancellous bone compartments that may contribute to progressive skeletal deformation. The present study provides insight into skeletal alterations associated with mcEDS-CHST14 and highlights a broader role of DS in maintaining bone structure and strength.
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