ReviewFrontiers in endocrinology2023
Liver-bone crosstalk in non-alcoholic fatty liver disease: Clinical implications and underlying pathophysiology.
Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 34 citations in OpenAlex.
- Reprogramming bone homeostasis: The recoupling-oriented framework of bidirectional regulation strategies for osteoporosis.iScience · 2026Review
- Inulin alleviates metabolic dysfunction-associated steatotic liver disease-induced bone loss potentially by activating the Nrf2/GPX4 signaling pathway.Molecular and cellular biochemistry · 2026Article
- Mechanistic insights and evidence-based management of metabolic dysfunction-associated steatotic liver disease (MASLD; formerly NAFLD) through combined diet and exercise interventions: an evidence-based narrative review.Journal of clinical biochemistry and nutrition · 2026Review
- Identification of the critical immune-related drivers shared by non-alcoholic fatty liver disease and osteoporosis.Cellular and molecular life sciences : CMLS · 2026Article
- Dynamic modelling of liver-bone axis: A microphysiological approach to hepatic osteodystrophy.Bioactive materials · 2026Article
- FXR in bone metabolism: An emerging regulator.iScience · 2026Review
- Article
- Beyond the Brain: Exploring the multi-organ axes in Parkinson's disease pathogenesis.Journal of advanced research · 2026Review
- LncRNA TUG1 promotes osteogenic differentiation of human umbilical cord mesenchymal stem cells by regulating miR-138/SIRT1 axis.Journal of orthopaedic surgery and research · 2026Article
- Alcohol consumption exacerbates high-fat diet-mediated disruptions in myelopoiesis and osteoclastogenesis in mouse models of metabolic dysfunction-associated liver diseases.Frontiers in endocrinology · 2026Article
- Long-term Western diet feeding impairs hepatic vitamin D metabolism and promotes bone loss in mice.EXCLI journal · 2026Article
- Anoctamin 5 mutation leads to abnormal bone homeostasis of GDD by regulating AMPK-dependent glucose metabolism.Frontiers in endocrinology · 2026Article
- Article
- Osteopontin: a central hub in the pathogenesis and therapeutic intervention of liver disease.Annals of medicine · 2025Review
- Hepatic osteodystrophy: An underrecognized metabolic bone disease.World journal of hepatology · 2025Review
- Sexual dimorphism of MASLD-driven bone loss.Scientific reports · 2025Article
- Exploring the Bone-Liver Axis: Impact of Acute Ethanol Intoxication on Post-Traumatic Liver Inflammation and Damage Following Femur Fracture.International journal of molecular sciences · 2025Article
- Oxidative stress-induced circSOD2 inhibits osteogenesis through sponging miR-29b in metabolic-associated fatty liver disease.World journal of gastroenterology · 2025Article
- Liver function linked to bone health: A bibliometric of the liver-bone axis.World journal of hepatology · 2025Article
- Kangshujiangu granules improve NAFLD via cross-organ autophagy activation shared with osteoporosis.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is a common complication of many types of chronic liver diseases (CLDs), such as cholestatic liver disease, viral hepatitis, and alcoholic liver disease. Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent metabolic liver disease, affecting almost one third of adults around the world, and is emerging as the dominant cause of CLDs. Liver serves as a hub for nutrient and energy metabolism in the body, and its crosstalk with other tissues, such as adipose tissue, heart, and brain, has been well recognized. However, much less is known about the crosstalk that occurs between the liver and bone. Moreover, the mechanisms by which CLDs increase the risk for osteoporosis remain unclear. This review summarizes the latest research on the liver-bone axis and discusses the relationship between NAFLD and osteoporosis. We cover key signaling molecules secreted by liver, such as insulin-like growth factor-1 (IGF-1), fibroblast growth factor 21 (FGF21), insulin-like growth factor binding protein 1 (IGFBP1), fetuin-A, tumor necrosis factor-alpha (TNF-α), and osteopontin (OPN), and their relevance to the homeostasis of bone metabolism. Finally, we consider the disordered liver metabolism that occurs in patients with NAFLD and how this disrupts signaling to the bone, thereby perturbing the balance between osteoclasts and osteoblasts and leading to osteoporosis or hepatic osteodystrophy (HOD).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.