ArticleCell proliferation2026
Unexpected Promotion of Bone Regeneration by Inhibition of BMPR1A-Mediated BMP Signalling.
Zihao Zhou, Yun Zhai, Xiaochen Liu, Jiaojiao Shao, Jiani Zhou, Zhaoyang Li, Jiale He, Shuxian Lin, Qi Zhang
Abstract read
In one paragraphArticle in Cell proliferation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
9 authors.
Zihao ZhouShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Endodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Yun ZhaiShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Prosthodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Xiaochen LiuShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Endodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0001-6252-4246 Jiaojiao ShaoShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Endodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Jiani ZhouShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Endodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Zhaoyang LiShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Endodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Jiale HeShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Endodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Shuxian LinShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Prosthodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0001-6944-5604 Qi ZhangShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Endodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0002-4549-9760 Funding
National Natural Science Foundation of China 82170945National Natural Science Foundation of China 82370950National Natural Science Foundation of China 82401093
6 · The paper itselfAbstract
Bone morphogenetic protein (BMP) signalling plays a pivotal role in bone regeneration by regulating osteoprogenitor cell (OPC) function, and BMPs have been widely used in clinical treatment. However, their limited specificity for OPCs often lead to side effects, highlighting that the regulatory mechanisms of BMP signalling remain to be further elucidated. BMPR1A, a key type I BMP receptor, has emerged as a critical regulator of bone development, yet its precise role in bone regeneration and downstream mechanisms remains unclear. Using OPC-specific conditional knockout (cKO) and constitutively activated (CA) BMPR1A mouse, we found conditional knockout of BMPR1A in OPCs during the first 2 weeks of healing significantly accelerated bone regeneration. At the cellular level, BMPR1A knockout promoted the proliferation of OPCs, thereby accelerating bone regeneration in cKO mice. Mechanistically, BMPR1A knockout reduced ID1 expression, releasing its inhibition of TCF3, which in turn induced GNG4 expression and ultimately activated the PI3K-AKT pathway. Finally, a double-knockdown cell line further demonstrated the role of the BMPR1A-ID1-TCF3-GNG4 signalling axis. This study reveals the function and mechanism of BMPR1A in bone regeneration and provides new insights for more precise BMP-targeted strategies.
Indexed as
Bone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsBone RegenerationSignal TransductionAnimalsCell ProliferationInhibitor of Differentiation Protein 1MiceMice, KnockoutPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBmpr1a protein, mouseBone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsIdb1 protein, mouseInhibitor of Differentiation Protein 1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBMPR1Abone regenerationOsteoprogenitor cellsproliferationtargeted BMP regulation
Identifiers
PMID41940494
PMCPMC13325999
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