ArticleNature communications2025
Snhg18 regulates Yap subcellular localization to maintain bone homeostasis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Review
- Disruption of YAP biomolecular condensates by mechanical stress drives intervertebral disc vascularization.Science advances · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
Osteoporosis treatments commonly mitigate bone loss but rarely restore lost bone mass. Yes-associated protein (Yap) nuclear translocation is crucial for the osteogenic differentiation of bone marrow stromal cells (BMSCs), but is disrupted by many factors under osteoporotic conditions. Long non-coding RNAs (lncRNAs) regulate BMSCs differentiation and Yap localization across diseases, exhibiting tissue- and cell-specific effects. However, their role in aberrant Yap signaling within BMSCs under osteoporosis remains unclear. Here, we identify small nucleolar RNA host gene 18 (lnc-Snhg18), a functionally conserved lncRNA enriched in the osteolineage of leptin receptor-positive (LepR⁺) cells within bone, as a key regulator promoting osteogenesis. Mechanistically, lnc-Snhg18 directly binds Caveolin-1 (Cav1) and 14-3-3 eta protein (Ywhah), facilitating Cav1-Ywhah complex formation, thereby disrupting the Ywhah-Yap interaction and enabling Yap nuclear translocation. Knockout of lnc-Snhg18 in LepR⁺ cells accelerates bone loss and traps Yap in the cytoplasm, while its delivery restores bone mass and Yap signaling in osteoporosis models. These findings identify lnc-Snhg18 as a promising therapeutic target for osteoporosis and related disorders.
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Registered trials
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