ArticleCell metabolism2022
Defects in a liver-bone axis contribute to hepatic osteodystrophy disease progression.
Article in Cell metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 111 citations in OpenAlex.
- Bioactive glasses-mediated ion therapy ameliorates hepatic osteodystrophy by reprogramming the liver-bone axis.Bioactive materials · 2027Article
- Tibial bone compression promotes recovery after brain injury through osteocyte PIEZO1.Nature neuroscience · 2026Article
- Multifunctional scaffold inspired by hepatocyte exosomes promotes bone regeneration by regulating osteogenic differentiation via PI3K/AKT pathway.Materials today. Bio · 2026Article
- Medicine-food homologous bioactives in metabolic dysregulation-associated osteoporosis: a review of preclinical evidence and potential liver-bone and gut-bone actions.Chinese medicine · 2026Review
- Clinical insights into the association between chronic liver disease and osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Review
- The liver-bone axis: an emerging player in disease pathogenesis and therapeutic intervention.Science China. Life sciences · 2026Review
- Inhibiting hepatocytes MAGL alleviates osteoporosis caused by high-fat diet-induced liver fibrosis in male mice.Journal of the Endocrine Society · 2026Article
- Liposomal multimodal theranostics for bone disorders: from rational responsive delivery and biomimetic strategies to clinical translation.Journal of nanobiotechnology · 2026Review
- A multiparameter model (OsteoSC-M3) for early detection and risk stratification of osteoporosis in women: a multicentre cohort study in China.EClinicalMedicine · 2026Article
- Targeting adipocyte ESRRA alleviates osteoarthritis via interrupting inter-organelle crosstalk of complement C3-CFD-MAC cascade.Bone research · 2026Article
- Dynamic modelling of liver-bone axis: A microphysiological approach to hepatic osteodystrophy.Bioactive materials · 2026Article
- [Liver-bone axis: novel mechanisms and strategies for MAFLD regulation].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Article
- Advanced bone-targeted nanomaterials for the systemic treatment of osteoporosis.Regenerative biomaterials · 2026Review
- Aberrant Cholesterol Metabolism Caused by Decreased Lecithin: Cholesterol Acyltransferase Promoted Hepatocarcinogenesis.Journal of hepatocellular carcinoma · 2026Article
- MAFLD and impaired bone formation in children: association with reduced serum LCAT.Frontiers in cell and developmental biology · 2026Article
- MAFLD is associated with lower bone mineral density in patients with type 2 diabetes: an exploratory cross-sectional analysis of a potential indirect association with HOMA-IR.Frontiers in medicine · 2026Article
- Organoids and organs-on-chips for accelerating R&D and clinical translation in Orthopaedics: Emerging opportunities and regulatory pathways.Journal of orthopaedic translation · 2026Review
- Association between HBV DNA levels and bone mineral density in antiviral-naive chronic hepatitis B patients.Frontiers in endocrinology · 2026Article
- Liver-eye axis in metabolic syndrome: integrated evidence from mendelian randomization, single-cell sequencing, and clinical sample validation.Frontiers in endocrinology · 2026Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic osteodystrophy (HOD) is a metabolic bone disease that is often associated with chronic liver disease and is marked by bone loss. Here, we demonstrate that hepatic expression of the phosphatase PP2Acα is upregulated during HOD, leading to the downregulation of expression of the hepatokine lecithin-cholesterol acyltransferase (LCAT). Loss of LCAT function markedly exacerbates the bone loss phenotype of HOD in mice. In addition, we found that alterations in cholesterol levels are involved in the regulation of osteoblast and osteoclast activities. We also found that LCAT improves liver function and relieves liver fibrosis in the mouse HOD model by promoting reversal of cholesterol transport from the bone to the liver. In summary, defects in a liver-bone axis occur during HOD that can be targeted to ameliorate disease progression.
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