1α,25-(OH)2-D3 promotes osteoclast-precursor autophagy and osteoclast differentiation by promoting BECN1 transcription
- 1Fuzhou Second General Hospital, Department of Orthopedics, Fuzhou, China.
- 2Affiliated Jiangyin Hospital of Xuzhou Medical University, Department of Orthopedics, Jiangyin, China.
Abstract
1α,25-(OH)2-D3 can promote autophagy of osteoclast precursors (OCPs), resulting in its pro-osteoclastogenic effect, which limits its anti-osteoporotic efficacy. To address the above challenges, we need to explore the targets of autophagy-enhancing effect of 1α,25-(OH)2-D3. These results showed that 1α,25-(OH)2-D3 promoted the expression of BECN1 mRNA and Beclin1 protein in OCPs under RANKL induction. Furthermore, 1α,25-(OH)2-D3 enhances p65 phosphorylation and nuclear translocation. The lentiviral-mediated silencing of both BECN1 and p65 impeded the facilitation of 1α,25-(OH)2-D3 on osteoclast differentiation and OCP autophagy. Moreover, p65 silencing blocked the enhancement of BECN1 mRNA expression and Beclin1 protein expression by 1α,25-(OH)2-D3. In conclusion, 1α,25-(OH)2-D3 enhances Beclin1-dependent autophagy in OCPs by promoting BECN1 transcription, thereby promoting osteoclast differentiation; this indicates that the therapeutic strategies for BECN1 or p65 targeted inhibition have the potential to optimize the anti-osteoporotic function of 1α,25-(OH)2-D3.
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BibTeX
@article{li20261α25oh2d3,
title = {{1α,25-(OH)2-D3 promotes osteoclast-precursor autophagy and osteoclast differentiation by promoting BECN1 transcription}},
author = {Xi Li and Hui Liu and Yunrong Zhu},
journal = {Genetics and Molecular Biology},
year = {2026},
month = oct,
doi = {10.1590/1678-4685-gmb-2025-0284},
url = {https://doi.org/10.1590/1678-4685-gmb-2025-0284},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - 1α,25-(OH)2-D3 promotes osteoclast-precursor autophagy and osteoclast differentiation by promoting BECN1 transcription
AU - Xi Li
AU - Hui Liu
AU - Yunrong Zhu
PY - 2026
DA - 2026/10/23
JO - Genetics and Molecular Biology
DO - 10.1590/1678-4685-gmb-2025-0284
UR - https://doi.org/10.1590/1678-4685-gmb-2025-0284
AB - 1α,25-(OH)2-D3 can promote autophagy of osteoclast precursors (OCPs), resulting in its pro-osteoclastogenic effect, which limits its anti-osteoporotic efficacy. To address the above challenges, we need to explore the targets of autophagy-enhancing effect of 1α,25-(OH)2-D3. These results showed that 1α,25-(OH)2-D3 promoted the expression of BECN1 mRNA and Beclin1 protein in OCPs under RANKL induction. Furthermore, 1α,25-(OH)2-D3 enhances p65 phosphorylation and nuclear translocation. The lentiviral-mediated silencing of both BECN1 and p65 impeded the facilitation of 1α,25-(OH)2-D3 on osteoclast differentiation and OCP autophagy. Moreover, p65 silencing blocked the enhancement of BECN1 mRNA expression and Beclin1 protein expression by 1α,25-(OH)2-D3. In conclusion, 1α,25-(OH)2-D3 enhances Beclin1-dependent autophagy in OCPs by promoting BECN1 transcription, thereby promoting osteoclast differentiation; this indicates that the therapeutic strategies for BECN1 or p65 targeted inhibition have the potential to optimize the anti-osteoporotic function of 1α,25-(OH)2-D3.
SN - 1415-4757
SN - 1678-4685
ER -