ArticleRegenerative therapy2023
Acyl-protein thioesterase1 alleviates senile osteoporosis by promoting osteoblast differentiation via depalmitoylation of BMPR1a.
Article in Regenerative therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of palmitoylation modifications in the regulation of bone cell function, bone homeostasis, and osteoporosis.Bone & joint research · 2025Pooled it
- Protein acylation and bone metabolism: bidirectional crosstalk linking metabolic reprogramming to skeletal homeostasis.Journal of molecular histology · 2026Review
- Targeting post-translational modifications: novel insights into bone metabolic diseases.Journal of advanced research · 2026Review
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Article
- Skeletal phenotypes and molecular mechanisms in aging mice.Zoological research · 2024Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Senile osteoporosis (SOP) is an aging-related disease. The depalmitoylating enzyme Acyl-protein thiesterase1 (APT1) is involved in disease regulation. This study explored the mechanism of APT1 in SOP. Methods: Eight-week-old SAMP6 mice were selected as SOP models and SAMR1 mice were controls, while osteoblasts were isolated from the femoral surface-soft tissues of SOP and control mice as Results: APT1 was under-expressed in osteoblasts of bone tissue in SOP mice and mainly localized in osteoblasts. SOP mice manifested increased bone marrow cavity and bone trabecular space, thinned trabecular bone, decreased BMD, maximum elastic stress, maximum load, and reduced OPG-positive osteoblasts in bone tissues, which were averted by APT1 overexpression, thus alleviating SOP. APT1 overexpression increased osteoblast calcium nodules, ALP activity, OD-related protein levels, and cell proliferation. In mechanism, APT1 overexpression inhibited BMPR1a palmitoylation in SOP mouse osteoblasts and activated the BMP/Smad pathway, thus promoting OD. Conclusion: APT1 activated the BMP/Smad pathway and promoted OD by regulating BMPR1a depalmitoylation, thus alleviating mouse SOP.
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