ArticleCellular and molecular life sciences : CMLS2022
Impairment of APPL1/Myoferlin facilitates adipogenic differentiation of mesenchymal stem cells by blocking autophagy flux in osteoporosis.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- T-Cadherin Finetunes Proliferation-Differentiation During Adipogenesis via PI3K-AKT Signaling Pathway.International journal of molecular sciences · 2025Article
- Mechanistic Insights Into GDFMD-Mediated Inhibition of Liver Fibrosis via miRNA-29b-3p Upregulation in Wilson's Disease.Mediators of inflammation · 2025Article
- Exploring the association between circadian rhythms and osteoporosis: new diagnostic and therapeutic targets identified via machine learning.Frontiers in molecular biosciences · 2025Article
- circNDUFA13 stimulates adipogenesis of bone marrow-derived mesenchymal stem cells via interaction with STAT3.Scientific reports · 2024Article
- Regulation of mesenchymal stem cell differentiation by autophagy.Open medicine (Warsaw, Poland) · 2024Review
- Novel perspectives on autophagy-oxidative stress-inflammation axis in the orchestration of adipogenesis.Frontiers in endocrinology · 2024Review
- Reduced APPL1 impairs osteogenic differentiation of mesenchymal stem cells by facilitating MGP expression to disrupt the BMP2 pathway in osteoporosis.The Journal of biological chemistry · 2023Article
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
An imbalance of human mesenchymal stem cells (hMSCs) adipogenic and osteogenic differentiation is crucial in the pathogenesis of osteoporosis, and elucidation of the underlying mechanism is urgently needed. APPL1, an adaptor protein of the adiponectin receptor, was recently shown to be closely related to bone mass. However, the role of APPL1 in the imbalance of hMSC differentiation in osteoporosis is unclear. Therefore, we aimed to explore the mechanisms by which APPL1 alters hMSCs adipogenic differentiation in osteoporosis. Here, we found that APPL1 expression was downregulated in elderly patients with osteoporosis and in mouse osteoporosis model. APPL1 negatively regulated hMSC adipogenic differentiation in vivo and in vitro. Mechanistically, by enhancing ubiquitination-mediated Myoferlin degradation, downregulated APPL1 expression increased the risk of lysosome dysfunction during hMSCs adipogenic differentiation. Lysosomal dysfunction inhibited autophagy flux by suppressing autophagosome degradation and promoted hMSC differentiation towards the adipocyte lineage. Our findings suggest that APPL1/Myoferlin downregulation promoted hMSCs adipogenic differentiation by inhibiting autophagy flux, further impairing the balance of hMSCs adipogenic and osteogenic differentiation in osteoporosis; the APPL1/ Myoferlin axis may be a promising diagnostic and therapeutic target for osteoporosis.
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