ArticleNature communications2018
Vagus-macrophage-hepatocyte link promotes post-injury liver regeneration and whole-body survival through hepatic FoxM1 activation.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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Who cites it
68 citing papers in PubMed, 108 citations in OpenAlex.
- Hepatic neurons and metabolically induced liver dysfunction.Nature reviews. Endocrinology · 2026Review
- Hypothalamic Control of Liver Health and Disease: From Circuits to Pathophysiology and Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Proximal labeling of the Golgi secretome reveals fat body-derived humoral factors in Drosophila disc regeneration.The Journal of biological chemistry · 2026Article
- Identification of Foxm1 as a critical regulator for metabolic dysfunction-associated steatotic liver disease by epigenomic and transcriptional profiling.Cell insight · 2026Article
- Systemic and metabolic control of liver regeneration.Trends in endocrinology and metabolism: TEM · 2026Review
- Liver-pancreas communication in disease and drug development.Acta pharmaceutica Sinica. B · 2026Review
- Biological fundamental functional units of meridians: mechanosensitive ion channels.Frontiers in medicine · 2026Review
- Role of central and peripheral serotonin in liver physiology and diseases.Theranostics · 2026Review
- Liver Innervation in Health and Disease: Neuroimmune-Neurovascular Interface and Future Therapeutic Implications.Biomedicines · 2025Review
- Splenectomy reduces shear stress and inflammation in liver endothelial cells during regeneration after partial hepatectomy in mice.Scientific reports · 2025Article
- Review
- Redox-dependent liver gluconeogenesis impacts different intensity exercise in mice.Nature metabolism · 2025Article
- Neural bridging achieves transcutaneous regulation of vagus nerve function and treatment of depressive disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- CpG-oligodeoxynucleotides challenged macrophages ameliorate acetaminophen induced liver injury by activating TLR9/IRG1/itaconate metabolic pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Integrating neuroscience and oncology: neuroimmune crosstalk in the initiation and progression of digestive system tumors.Molecular cancer · 2025Review
- Roles of Peripheral Nerves in Tumor Initiation and Progression.International journal of molecular sciences · 2025Review
- Colonic inflammation triggers β cell proliferation during obesity development via a liver-to-pancreas interorgan mechanism.JCI insight · 2025Article
- Inhibition of miR-142-3p promotes intestinal epithelial proliferation and barrier function after ischemia/reperfusion injury by targeting FoxM1.Molecular and cellular biochemistry · 2025Article
- Rspo3-mediated metabolic liver zonation regulates systemic glucose metabolism and body mass in mice.PLoS biology · 2025Article
- Liver Cancer Neuroscience: Regulating Liver Tumors via Selective Hepatic Vagotomy.Methods and protocols · 2024Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
Abstract
The liver possesses a high regenerative capacity. Liver regeneration is a compensatory response overcoming disturbances of whole-body homeostasis provoked by organ defects. Here we show that a vagus-macrophage-hepatocyte link regulates acute liver regeneration after liver injury and that this system is critical for promoting survival. Hepatic Foxm1 is rapidly upregulated after partial hepatectomy (PHx). Hepatic branch vagotomy (HV) suppresses this upregulation and hepatocyte proliferation, thereby increasing mortality. In addition, hepatic FoxM1 supplementation in vagotomized mice reverses the suppression of liver regeneration and blocks the increase in post-PHx mortality. Hepatic macrophage depletion suppresses both post-PHx Foxm1 upregulation and remnant liver regeneration, and increases mortality. Hepatic Il-6 rises rapidly after PHx and this is suppressed by HV, muscarinic blockade or resident macrophage depletion. Furthermore, IL-6 neutralization suppresses post-PHx Foxm1 upregulation and remnant liver regeneration. Collectively, vagal signal-mediated IL-6 production in hepatic macrophages upregulates hepatocyte FoxM1, leading to liver regeneration and assures survival.
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Registered trials
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.