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FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging
Open accessAbstract
A hallmark of aged mesenchymal stem/progenitor cells (MSCs) in bone marrow is the pivot of differentiation potency from osteoblast to adipocyte coupled with a decrease in self-renewal capacity. However, how these cellular events are orchestrated in the aging progress is not fully understood. In this study, we have used molecular and genetic approaches to investigate the role of forkhead box P1 (FOXP1) in transcriptional control of MSC senescence. In bone marrow MSCs, FOXP1 expression levels declined with age in an inverse manner with those of the senescence marker p16INK4A. Conditional depletion of Foxp1 in bone marrow MSCs led to premature aging characteristics, including increased bone marrow adiposity, decreased bone mass, and impaired MSC self-renewal capacity in mice. At the molecular level, FOXP1 regulated cell-fate choice of MSCs through interactions with the CEBPβ/δ complex and recombination signal binding protein for immunoglobulin κ J region (RBPjκ), key modulators of adipogenesis and osteogenesis, respectively. Loss of p16INK4A in Foxp1-deficient MSCs partially rescued the defects in replication capacity and bone mass accrual. Promoter occupancy analyses revealed that FOXP1 directly represses transcription of p16INK4A. These results indicate that FOXP1 attenuates MSC senescence by orchestrating their cell-fate switch while maintaining their replicative capacity in a dose- and age-dependent manner.
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“Ageing and genotoxic stress induce cellular senescence of these stem cells 96,97 and osteoprogenitor cells, 98,99 with subsequent decline in the functions of these cells in both mice and humans.100”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [98]
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BackgroundLRRC15 expression indicates high level of stemness regulated by TWIST1 in mesenchymal stem cells
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“Similarly, Li et al. demonstrated that MSCs overexpressing forkhead box P1 (FOXP1) played a crucial role in cell cycle regulation, enhancing MSCs self-renewal by suppressing p16INK4A activation [128].”
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“Our previous studies revealed an age-dependent role for FOXP1 in maintaining MSC self-renewal potency through direct transcriptional repression of p16, a tumor suppressor which plays an important role in cell cycle regulation [34].”
BackgroundResultInfluentialStromal Co-Cultivation for Modeling Breast Cancer Dormancy in the Bone Marrow
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“FOXP1 expression declines with age in bone MSCs, a trend inversely correlated with the senescence marker p16INK4a, the transcription of which it directly represses [38].”
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ResultLi, Q., Liu, W.-J., Zhang, Y.-H., Jin, J.-H., Ji, P.-F., Yuan, Z., Zhang, Y.-B., Feng, P., Wu, Y.-F., Shen, H.-Y., et al. (2025) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-024-05566-9 · Cited by 7
“Previous studies have shown that a key imbalance between bone mineralization and adipose tissue in bone marrow plays an important role in OP development [4, 5].”
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“Specifically, the senescence-associated increase in p16 INK4a expression with aging in BMSCs is matched with a decline in Foxp1 , a transcriptional repressor of genes that plays a central role in adipogenesis (e.g., Pparg , Cebpa , Fabp4 ) [32, 33].”
Role of myofiber-specific FoxP1 in pancreatic cancer-induced muscle wasting
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“For example, FOXP1 expression in mesenchymal stem/progenitor cells (MSCs) decreased with age in an inverse relationship with the senescence marker p16INK4A (Li et al. 2017).”
Zhang, S., You, Y., Li, Y., Yuan, H., Zhou, J., Tian, L., Liu, Y., Wang, B., & Zhu, E. (2023) · The FASEB Journal · doi:10.1096/fj.202301153r · Cited by 5
“35 In adipogenesis, Foxa3 promotes adipocyte differentiation by cooperating with C/EBPs to transcriptionally induce PPAR γ expression 36 ; Foxp1 suppresses adipocyte differentiation by interacting with C/EBP β / δ and RBPj κ 37 ; Foxo1 represses the expression and transcriptional activity of PPAR γ and C/EBPs or regul…”
BackgroundAngiopoietin-like 8 governs osteoblast-adipocyte lineage commitment during skeletal aging
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“Histochemical analysis was conducted in accordance with established protocols (9, 61).”
He, R., Xiao, C., Lei, W., Chen, G., Li, Y., & Luo, O. J. (2025) · BMC Biology · doi:10.1186/s12915-025-02484-5 · Cited by 5
“Defects or downregulated FOXP1 expression leads to aging in multiple tissues and organs, including mesenchymal stem cells [52–54].”
Targeting MCH Neuroendocrine Circuit in Lateral Hypothalamus to Protect Against Skeletal Senescence
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FOXP1 promotes osteoblast differentiation via regulation of TGF-β/ALK-5 pathway
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“Li et al. [93] demonstrated that the expression of forkhead box P1 in BMSCs decreases with age, and conditional deletion of Foxp1 in mouse BMSCs leads to premature aging, characterized by increased bone marrow fat, decreased bone mass, and impaired self-renewal of BMSCs.”
Applications of Nonviral Biomaterials for microRNA Transfection in Bone Tissue Engineering
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“The transcriptional inhibition mechanism of FOXP1 for p16INK4A is involved in the regulation of the fate of MSCs by FOXP1 [31].”
The mechanism of lncRNA SNHG1 in osteogenic differentiation via miR-497-5p/ HIF1AN axis
Lu, Y., Pan, K., Zhang, Y., Peng, J., Cao, D., & Li, X. (2023) · Connective Tissue Research · doi:10.1080/03008207.2023.2281321 · Cited by 2
“Diminished self-renewal and osteogenic lineage commitment in aging BMSCs can contribute to osteoporosis development 31,32 .”
BackgroundWafer, R., Tandon, P., & Minchin, J. E. N. (2025) · eLife · doi:10.7554/elife.107327 · Cited by 3
Lee, J., Lee, S., Kim, K., Park, K., & Park, K. (2019) · Stem Cell Research & Therapy · doi:10.1186/s13287-019-1137-9 · Cited by 1
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“…factor that regrates multiple differentiation pathways during development, negatively regulates VEGFR3 expression through the suppression of Tumor necrosis factor superfamily 15 (TNFSF15) which belongs to the tumor necrosis factor ligand family and serve as an angiogenesis inhibitor [35, 36].”
BackgroundFOXP1 contributes to murine hematopoietic stem cell functionality
Levavasseur, F., Oussous, S., Framarini, A., Boussaid, I., Gou, P., Tuerdi, Z., Boueya, I. L., Hoffner, H., de Almeida, M., Gall, M. L., et al. (2025) · Experimental Hematology · doi:10.1016/j.exphem.2025.104815 · Cited by 1
“…pathways, including embryonic stem cell pluripotency [18], hair follicle stem cell quiescence [19], mesenchymal stem cell commitment [20], adipocyte differentiation [21], lung epithelial cell-fate determination [22,23], cardiomyocyte proliferation [24,25] and neuronal activity…”
Mesenchymal Stem Cell Aging in the Bone Marrow
Ho, Y., & Méndez‐Ferrer, S. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.11571-5
Orchestration of alternative splicing regulates bone marrow mesenchymal stem cells fate during agingPreprint
Xiao, Y., Cai, G., Xu, F., Guo, Q., Huang, Y., Su, T., Li, C., Luo, X., Zheng, Y., & Yang, M. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.05.27.493685
Osteoporoz ve Periodontal Hastalıklar Arasındaki İlişki Üzerine Derleme
Karaaslan, R., Bağış, N., & Fentoğlu, Ö. (2024) · Süleyman Demirel Üniversitesi Sağlık Bilimleri Dergisi · doi:10.22312/sdusbed.1398573
Mesenchymal Stem Cells and Sarcoma
Hatina, J., Kripnerová, M., Dejmek, J., Dolejšová, M., & Pešta, M. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-15717-2.00116-5
Schonk, M. M., Ducharme, J. B., Neyroud, D., Nosacka, R. L., Tucker, H. O., Judge, S. M., & Judge, A. R. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.09.17.613547
“FoxP1 has been shown to regulate proliferation and differentiation of various cells types, including immune cells 9 , mesenchymal stem cells 10 , adipocytes 11 and cardiomyocytes 12,13 .”
BackgroundАлександровна, С. Т., Учасова, Е. Г., Dyleva, Y. A., Belik, E. V., & Gruzdeva, O. V. (2024) · Fundamental and Clinical Medicine · doi:10.23946/2500-0764-2024-9-4-95-106
Jiang, J., Li, D., Cui, D., Wan, Y., Zhou, P., Cui, X., & Yu, H. (2025) · Biochemical Genetics · doi:10.1007/s10528-025-11099-y
“The weakened ability of BMSCs to differentiate into osteoblasts results in decreased bone mass and increased fat accumulation in the bone marrow cavity, both being critical pathogenic mechanisms in OS (Moerman et al. 2004; Li et al. 2017).”
Wafer, R., Tandon, P., & Minchin, J. E. N. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.20.649706
“We adapted the morphology value framework developed by the Arner lab for human adipose ( Li et al., 2017 ) and observed strikingly similar relationships in zebrafish SAT, including a curvilinear relationship between LD size and depot size and an inverse correlation between LD number and LD size.”
Wafer, R., Tandon, P., & Minchin, J. E. N. (2025) · eLife · doi:10.7554/elife.107327.1
miR-34a-5p targets Foxp1 to promote osteoclast differentiation and accelerate fracture healingPreprint
Ding, C., Zhang, H., Liu, P., Ding, W., Xu, M., & Meng, B. (2025) · Research Square · doi:10.21203/rs.3.rs-7121624/v1
Ling, S., Chen, T., Wang, S., Zhang, W., Zhou, R., Xia, X., Yao, Z., Fan, Y., Ning, S., Liu, J., et al. (2023) · Figshare · doi:10.6084/m9.figshare.23803219
Qiao, H., Mei, J., Yuan, K., Zhang, K., Zhou, F., Tang, T., & Zhao, J. (2022) · Figshare · doi:10.6084/m9.figshare.20317834
Ding, C., Zhang, H., Liu, P., Ding, W., Xu, M., & Meng, B. (2025) · Thermochimica Acta · doi:10.1016/j.tca.2025.180204
Effects of autophagy modulators on the therapeutic efficacy of multipotent mesenchymal stromal cells
Ivanov, V. A., Grebnev, D. Y., & Maklakova, I. Y. (2026) · Kazan medical journal · doi:10.17816/kmj693214
“1 [18–24].”
Wafer, R., Tandon, P., & Minchin, J. E. N. (2026) · eLife · doi:10.7554/elife.107327.2
Epigenetic transcriptional regulation of skeletal aging: The emerging role of m6A methylation
Song, C., Song, G., Zhang, S., Zhao, H., Wen, Z., Chen, Y., Chen, X., Liu, B., Ni, Q., & Fan, D.-P. (2026) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2026.101088 · Cited by 1
Wen, X., Cui, J., Wei, X., Zhang, G., Zhang, Y., Liu, G., Li, H., Qi, M., Li, D., Liu, C., et al. (2026) · Chemical Engineering Journal · doi:10.1016/j.cej.2026.183518
Metadata
- Authors
- Li, H., Liu, P., Xu, S., Li, Y., Dekker, J. D., Li, B., Fan, Y., Zhang, Z., Hong, Y., Yang, G., Tang, T., Ren, Y., Tucker, H. O., Yao, Z., & Guo, X.
- Affiliations
- Shanghai Jiao Tong University (CN)
- Fudan University (CN)
- The University of Texas at Austin (US)
- Shanghai Sixth People's Hospital (CN)
- Nanjing First Hospital (CN)
- Corresponding author
- Guo, Xizhi
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2017-02-27
- Volume
- 127
- Issue
- 4
- Pages
- 1241-1253
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC5373872
- OpenAlex
- W2591050028
- Cited by
- 180
- References
- 74
- Citations by year
- 2026: 8 · 2025: 22 · 2024: 24 · 2023: 33 · 2022: 27 · 2021: 18 · 2020: 18 · 2019: 9 · 2018: 18 · 2017: 3
- FWCI
- 7.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Lymphoma Research Foundation (300463)
- Cancer Prevention and Research Institute of Texas (RP120459, RP120348 and RP120459, RP120348)
- National Natural Science Foundation of China (973 Program, 31171396, 31100624, 2012CB966903, 31271553, 81421061, 81200586, 2014CB942902, R01CA31534)
- National Institutes of Health (31100624, 31271553, 2014CB942902, 31171396, 81421061, 2012CB966903)
- National Key Research and Development Program of China (31271553, 2012CB966903, R01CA31534, 31100624, 31171396, 2014CB942902, 81421061)
- National Cancer Institute (R01CA031534)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Mesenchymal stem cell research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Keywords
- FOXP1, mesenchymal stem cells, skeletal aging, cellular senescence, p16INK4a, bone marrow adiposity, bone formation, adipogenesis, lineage commitment, transcriptional repression, replicative capacity, bone mass
- MeSH terms
- Animals, Bone Marrow Cells, Cell Line, Humans, Osteogenesis, Repressor Proteins, Cellular Senescence, Mice, Knockout, Cyclin-Dependent Kinase Inhibitor p16, CCAAT-Enhancer-Binding Protein-beta, Adipogenesis, Mice, CCAAT-Enhancer-Binding Protein-delta, Forkhead Transcription Factors, Mesenchymal Stem Cells
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