ArticleCellular and molecular life sciences : CMLS2025
ALG5 downregulation inhibits osteogenesis and promotes adipogenesis by regulating the N-glycosylation of SLC6A9 in osteoporosis.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Article
- Cellular signaling crosstalk between osteoporosis and diabetes: Common mechanisms and therapeutic targets (Review).Biomedical reports · 2026Review
- MSTNCells · 2026Article
- GlyT1 inhibition by ALX-5407 attenuates allograft rejection through suppression of Th1 cell differentiation.Frontiers in immunology · 2025Article
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11 authors.
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Abstract
Osteoporosis is characterized by decreased bone mass and accumulation of adipocytes in the bone marrow. The mechanism underlying the imbalance between osteoblastogenesis and adipogenesis in bone marrow mesenchymal stem cells (BMSCs) remains unclear. We found that ALG5 was significantly downregulated in BMSCs from osteoporotic specimens. ALG5 knockdown inhibited osteogenic differentiation and increased adipogenic differentiation of BMSCs. ALG5 deficiency diminished the N-glycosylation of SLC6A9, thereby altering its protein stability and disrupting SLC6A9-mediated glycine uptake in BMSCs. ALG5 overexpression by adeno-associated virus serotype 9 (rAAV9) alleviated bone loss in OVX mice. Taken together, our findings suggest a novel role for the ALG5-SLC6A9-glycine axis in the imbalance of BMSC differentiation in osteoporosis. Moreover, we identify ALG5 overexpression as a potential therapeutic strategy for treating osteoporosis.
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