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Osteoporosis

SLC26A2 deficiency, matrix stiffness and mechanotransduction linked in osteoporosis

Nature Reviews Rheumatology volume 19, page 677 (2023)Cite this article

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Mutations in sulfation-related genes, including SLC26A2, are associated with a number of human skeletal diseases. However, the precise function of sulfation in bone cells and its relevance to bone mass has remained unclear. New research reveals that SLC26A2 deficiency in osteoblasts affects the pericellular matrix and the mechanical regulation of bone mass, and highlights mechanotranduction pathways that could be targeted as a therapeutic strategy to prevent bone loss.

In the study, genotype–phenotype correlation analyses revealed an association between SLC26A2 deficiency and osteoporotic phenotypes in humans and in mice. Characterization of Slc26a2 deficiency at various developmental stages in different mouse lines suggested that these phenotypes are caused by defective osteoblast maturation.

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References

Original article

  • Zheng, C. et al. Targeting sulfation-dependent mechanoreciprocity between matrix and osteoblasts to mitigate bone loss. Sci. Transl. Med. 15, eadg3983 (2023)

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  1. Nature Reviews Rheumatology http://www.nature.com/nrrheum/

    Sarah Onuora

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  1. Sarah Onuora
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Correspondence to Sarah Onuora.

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Onuora, S. SLC26A2 deficiency, matrix stiffness and mechanotransduction linked in osteoporosis. Nat Rev Rheumatol 19, 677 (2023). https://doi.org/10.1038/s41584-023-01041-0

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  • DOI: https://doi.org/10.1038/s41584-023-01041-0

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