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A Vitamin D Receptor/SMAD Genomic Circuit Gates Hepatic Fibrotic Response
Open accessAbstract
Liver fibrosis is a reversible wound-healing response involving TGFβ1/SMAD activation of hepatic stellate cells (HSCs). It results from excessive deposition of extracellular matrix components and can lead to impairment of liver function. Here, we show that vitamin D receptor (VDR) ligands inhibit HSC activation by TGFβ1 and abrogate liver fibrosis, whereas Vdr knockout mice spontaneously develop hepatic fibrosis. Mechanistically, we show that TGFβ1 signaling causes a redistribution of genome-wide VDR-binding sites (VDR cistrome) in HSCs and facilitates VDR binding at SMAD3 profibrotic target genes via TGFβ1-dependent chromatin remodeling. In the presence of VDR ligands, VDR binding to the coregulated genes reduces SMAD3 occupancy at these sites, inhibiting fibrosis. These results reveal an intersecting VDR/SMAD genomic circuit that regulates hepatic fibrogenesis and define a role for VDR as an endocrine checkpoint to modulate the wound-healing response in liver. Furthermore, the findings suggest VDR ligands as a potential therapy for liver fibrosis.
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“In an animal study, VDR -/-mice developed spontaneous liver fibrosis, thus indicating the importance of VDR in liver fibrosis and showing that VDR signaling regulates the inhibition of HSC activation.[95]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [95]
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“Briefly, VDR activation inhibits the signaling of a TGF-β/SMAD-dependent transcription response in HSCs.[95]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [95]
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Alonso-Merino, E., Martín Orozco, R., Ruíz-Llorente, L., Martínez-Iglesias, O. A., Velasco-Martín, J. P., Montero-Pedrazuela, A., Fanjul-Rodríguez, L., Contreras-Jurado, C., Regadera, J., & Aranda, A. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1506113113 · Cited by 108
Cystic Fibrosis–related Liver Disease
Debray, D., Narkewicz, M. R., Bodewes, F. A. J. A., Colombo, C., Housset, C., de Jonge, H. R., Jonker, J. W., Kelly, D. A., Ling, S. C., Poynard, T., et al. (2017) · Journal of Pediatric Gastroenterology and Nutrition · doi:10.1097/mpg.0000000000001676 · Cited by 108
Vitamin D Signaling in the Context of Innate Immunity: Focus on Human Monocytes
Carlberg, C. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02211 · Cited by 117
Vitamin D and the risk for cancer: A molecular analysis
Carlberg, C., & Velleuer, E. (2021) · Biochemical Pharmacology · doi:10.1016/j.bcp.2021.114735 · Cited by 114
Fedirko, V., Duarte‐Salles, T., Bamia, C., Trichopoulou, A., Aleksandrova, K., Trichopoulos, D., Trépo, E., Tjønneland, A. M., Olsen, A., Overvad, K., et al. (2014) · Hepatology · doi:10.1002/hep.27079 · Cited by 108
Yan, J., Tung, H., Li, S., Niu, Y., Garbacz, W. G., Lu, P., Bi, Y., Li, Y., He, J., Xu, M., et al. (2019) · Gastroenterology · doi:10.1053/j.gastro.2019.05.066 · Cited by 109
Primary Vitamin D Target Genes of Human Monocytes
Nurminen, V., Seuter, S., & Carlberg, C. (2019) · Frontiers in Physiology · doi:10.3389/fphys.2019.00194 · Cited by 106
The role of vitamin D and vitamin D binding protein in chronic liver diseases
Pop, T. L., Sîrbe, C., Benţa, G., Mititelu, A., & Grama, A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231810705 · Cited by 105
“Vitamin D administration reduces extracellular matrix deposition and attenuates fibrosis in animal models of chronic hepatic injury [16,54,59], but the ability to remediate already-established fibrosis is less promising.”
BackgroundThe Role and Mechanism of Oxidative Stress and Nuclear Receptors in the Development of NAFLD
Hong, T., Chen, Y., Li, X., & Lü, Y. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/6889533 · Cited by 110
Vitamin D and liver fibrosis: molecular mechanisms and clinical studies
Udomsinprasert, W., & Jittikoon, J. (2019) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.10.140 · Cited by 99
Stellate Cells in Tissue Repair, Inflammation, and Cancer
Sherman, M. H. (2018) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-100617-062855 · Cited by 104
Self-citationLade, A. G., Noon, L. A., & Friedman, S. L. (2013) · Current Opinion in Oncology · doi:10.1097/cco.0000000000000042 · Cited by 103
Metadata
- Authors
- Ding, N., Yu, R. T., Subramaniam, N., Sherman, M. H., Wilson, C., Rao, R., Leblanc, M., Coulter, S., He, M., Scott, C., Lau, S. L., Atkins, A. R., Barish, G. D., Gunton, J. E., Liddle, C., Downes, M., & Evans, R. M.
- Affiliations
- Salk Institute for Biological Studies (US)
- The University of Sydney (AU)
- Garvan Institute of Medical Research (AU)
- Corresponding author
- Downes, Michael
- Evans, Ronald M.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 153
- Issue
- 3
- Pages
- 601-613
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3673534
- OpenAlex
- W2144378498
- Cited by
- 622
- References
- 68
- Citations by year
- 2026: 26 · 2025: 24 · 2024: 38 · 2023: 51 · 2022: 39 · 2021: 48 · 2020: 57 · 2019: 54 · 2018: 52 · 2017: 55 · 2016: 57 · 2015: 53 · 2014: 49 · 2013: 19
- FWCI
- 37.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Heart, Lung, and Blood Institute (HL105278, K08HL092298, R01HL105278, HL-088093, P01HL088093)
- National Cancer Institute (CA014195, T32CA009370, P30CA014195, P30CA060553)
- National Institute of Diabetes and Digestive and Kidney Diseases (R37DK057978, DK057978, R01DK057978, R24DK090962, DK090962, P30DK063491)
- National Institute of Environmental Health Sciences (P42ES010337, ES 010337)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- vitamin D receptor, Smad3, liver fibrosis, hepatic stellate cells, TGF-β1 signaling, chromatin remodeling, fibrogenesis, wound healing, extracellular matrix deposition, VDR knockout mice
- MeSH terms
- Animals, Calcitriol, Fibrosis, Liver, Male, Mice, Inbred C57BL, Signal Transduction, Receptors, Calcitriol, Mice, Knockout, Mice, Rats, Smad3 Protein, Gene Regulatory Networks, Transforming Growth Factor beta1, Genome-Wide Association Study, Hepatic Stellate Cells, Transcriptome
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