sLZIP functions as a key modulator of bone remodeling by regulating the crosstalk between osteoblasts and osteoclasts.
Park S., Kim J., Ko J.
Animal Study, published in Exp Mol Med (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Exp Mol Med (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40025167
- PMCID
- PMC11958637
- DOI
- 10.1038/s12276-025-01414-3
- Citations
- 2
Abstract (original English)
Abstract Human small leucine zipper protein (sLZIP) regulates differentiation of both osteoblasts (OBs) and osteoclasts (OCs). However, the regulatory role of sLZIP in bone remodeling and its involvement in bone disorders remain unclear. In this study, we investigated the role of sLZIP in bone remodeling and its significance in the development of cell therapies for the treatment of bone diseases. sLZIP increased bone mass in an osteoporosis mouse model. However, bone mass was lower in mesenchymal stem cell-specific murine LZIP-1/2 knockout (Osx-LZIP-1/2 fl/fl ) mice than in control LZIP-1/2 fl/fl mice. Osx-LZIP-1/2 fl/fl mice showed delayed bone fracture healing in osteoporosis compared with control mice. Conditioned medium (CM) of OBs differentiated from adipose-derived stem cells (ADSCs) in Osx-LZIP-1/2 fl/fl mice attenuated OC formation and migration of bone marrow-derived macrophages. However, CM of OCs from sLZIP transgenic mice induced OB differentiation and migration. sLZIP regulates secretion of OC-derived sphingosine-1-phosphate, which induces OB differentiation. sLZIP also regulates OB-derived WNT16, which inhibits OC differentiation. Therefore, sLZIP functions as a key modulator of the crosstalk between OBs and OCs and promotes bone remodeling and fracture healing in osteoporosis. In addition, sLZIP-overexpressing ADSCs promoted bone formation and repair in osteoporo
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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