CoChat
Sign Up
Cited by 134Liver physiology and pathologyTissue Engineering and Regenerative MedicineOrgan Transplantation Techniques and Outcomes

The DOI matches its Crossref record; 833 of the 833 references it cites were found in a registry or an index.

Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics

Open access
Ma, Xiao, Huang, Tengda, Chen, Xiangzheng, Li, Qian, Liao, Mingheng, Fu, Li, Huang, Jiwei, Yuan, Kefei, Wang, Zhen, Zeng, Yong·2025·Signal Transduction and Targeted Therapy
DOI 10.1038/s41392-024-02104-8PMC PMC11806117
Open this paper in CoChat — free accountOpen PDF

Abstract

Liver repair and regeneration are crucial physiological responses to hepatic injury and are orchestrated through intricate cellular and molecular networks. This review systematically delineates advancements in the field, emphasizing the essential roles played by diverse liver cell types. Their coordinated actions, supported by complex crosstalk within the liver microenvironment, are pivotal to enhancing regenerative outcomes. Recent molecular investigations have elucidated key signaling pathways involved in liver injury and regeneration. Viewed through the lens of metabolic reprogramming, these pathways highlight how shifts in glucose, lipid, and amino acid metabolism support the cellular functions essential for liver repair and regeneration. An analysis of regenerative variability across pathological states reveals how disease conditions influence these dynamics, guiding the development of novel therapeutic strategies and advanced techniques to enhance liver repair and regeneration. Bridging laboratory findings with practical applications, recent clinical trials highlight the potential of optimizing liver regeneration strategies. These trials offer valuable insights into the effectiveness of novel therapies and underscore significant progress in translational research. In conclusion, this review intricately links molecular insights to therapeutic frontiers, systematically charting the trajectory from fundamental physiological mechanisms to innovative clinical applications in liver repair and regeneration.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/s41392-024-02104-8

Cites

833 of 833 references verified0 citation errors · 0 not checkable

Statistics

Figures

Fig. 1 Retrospective summary of research milestones in the field of liver repair and regeneration. The linear timeline shows outstanding contributions to the field in different eras. AI, artificial intelligence. The figure was generated with BioRender (https://biorender.com)
Fig. 1 Retrospective summary of research milestones in the field of liver repair and regeneration. The linear timeline shows outstanding contributions to the field in different eras. AI, artificial intelligence. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 2 Roles of liver cells during liver repair and regeneration. Different cell subsets regulate the proliferation of hepatocytes by secreting cytokines and chemokines. The arrows indicate a stimulatory effect on proliferation, and the T-arrows indicate an inhibitory effect. The dotted lines indicate dedifferentiation, differentiation or transdifferentiation. The circular dotted line indicates renewal. HSC hepatic stellate cell, LPC liver progenitor cell, BEC biliary epithelial cell, NKT natural killer T, DC dendritic cell, KC kupffer cell, MoMF monocyte-derived macrophage, ILC innate lymphoid cell, ALR, augmenter of liver regeneration, FGF fibroblast growth factor, HGF hepatocyte growth factor, IL interleukin, sIL-6R, soluble IL-6R, TGF-β transforming growth factor β, IFN-γ interferon-gamma, TNF-α tumor necrosis factor α, VEGF vascular endothelial growth factor, PDGF platelet-derived growth factor. The figure was generated with BioRender (https://biorender.com)
Fig. 2 Roles of liver cells during liver repair and regeneration. Different cell subsets regulate the proliferation of hepatocytes by secreting cytokines and chemokines. The arrows indicate a stimulatory effect on proliferation, and the T-arrows indicate an inhibitory effect. The dotted lines indicate dedifferentiation, differentiation or transdifferentiation. The circular dotted line indicates renewal. HSC hepatic stellate cell, LPC liver progenitor cell, BEC biliary epithelial cell, NKT natural killer T, DC dendritic cell, KC kupffer cell, MoMF monocyte-derived macrophage, ILC innate lymphoid cell, ALR, augmenter of liver regeneration, FGF fibroblast growth factor, HGF hepatocyte growth factor, IL interleukin, sIL-6R, soluble IL-6R, TGF-β transforming growth factor β, IFN-γ interferon-gamma, TNF-α tumor necrosis factor α, VEGF vascular endothelial growth factor, PDGF platelet-derived growth factor. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 3 Crosstalk among diverse cells during liver repair and regeneration. Interactions between hepatocytes, immune cells, and other liver cell types, facilitated by the signaling molecules, regulate the dynamic process of liver regeneration. The dots represent relay cells. The tail of the Y-shaped arrow represents a continuous path with the previous relay. The arrows indicate a stimulatory effect on proliferation, and the T-arrows indicate an inhibitory effect. The dotted lines indicate dedifferentiation, differentiation, or transdifferentiation. HSC hepatic stellate cell, LPC liver progenitor cell, BEC biliary epithelial cell, NKT natural killer T, KC kupffer cell, IL interleukin, TNF-α tumor necrosis factor α; VEGF, vascular endothelial growth factor, PDGF platelet-derived growth factor, TGF-β transforming growth factor β, CCL2, C-C motif chemokine ligand 2, CXCL1 C-X-C motif chemokine ligand 1, S1P sphingosine 1-phosphate, sIL-6R, soluble IL-6R. ICAM-1, intercellular adhesion molecule 1, OPN osteopontin. The figure was generated with BioRender (https://biorender.com)
Fig. 3 Crosstalk among diverse cells during liver repair and regeneration. Interactions between hepatocytes, immune cells, and other liver cell types, facilitated by the signaling molecules, regulate the dynamic process of liver regeneration. The dots represent relay cells. The tail of the Y-shaped arrow represents a continuous path with the previous relay. The arrows indicate a stimulatory effect on proliferation, and the T-arrows indicate an inhibitory effect. The dotted lines indicate dedifferentiation, differentiation, or transdifferentiation. HSC hepatic stellate cell, LPC liver progenitor cell, BEC biliary epithelial cell, NKT natural killer T, KC kupffer cell, IL interleukin, TNF-α tumor necrosis factor α; VEGF, vascular endothelial growth factor, PDGF platelet-derived growth factor, TGF-β transforming growth factor β, CCL2, C-C motif chemokine ligand 2, CXCL1 C-X-C motif chemokine ligand 1, S1P sphingosine 1-phosphate, sIL-6R, soluble IL-6R. ICAM-1, intercellular adhesion molecule 1, OPN osteopontin. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 4 Canonical signaling pathways involved in liver repair and regeneration. This diagram illustrates the key molecular components and regulatory mechanisms involved in different signaling pathways. RTK receptor tyrosine kinase, GPCR G-protein-coupled receptor, LGR leucine-rich repeat-containing G protein-coupled receptor, LRP low-density lipoprotein receptor-related protein, FZD frizzled, 5-HT 5-hydroxytryptamine. GLUT glucose transporter type, SMO smoothened, PTC patched, IL-6R, IL-6 receptor, gp130 glycoprotein 130, TNF-R, TNF receptor, TGFβ-R TGF-β receptor, PI3K phosphoinositide 3-kinase, AKT protein kinase B, mTORC1 mammalian target of rapamycin complex 1, WIP wild-type p53-induced phosphatase 1, S6K ribosomal S6 protein kinase, 4E-BP eukaryotic translation initiation factor 4E-binding protein, CXXC5 CXXC5-type zinc finger protein 5, DVL disheveled, ZNRF3, Zinc and Ring Finger 3, RNF43 Ring Finger Protein 43, TMEM9 transmembrane protein 9, APC adenomatous polyposis coli, GSK-3 glycogen synthase kinase 3, AXIN axis inhibition protein, CK1 casein kinase 1, AURKA aurora kinase A, MST ste20-like kinase, SAV salvador, LATS large tumor suppressor kinase, YAP Yes-associated protein, AMPK AMP-activated protein kinase, BRG1 brahma-related gene 1, CAR androstane receptor, PXR pregnane X receptor, PPARα peroxisome proliferator-activated receptor α, PFK1 phosphofructokinase-1, GLI zinc finger protein, SMAD suppressor of mothers against decapentaplegic, NOX4 NADPH oxidase 4, ROS reactive oxygen species, NICD Notch intracellular domain, TCF T-cell factor, LEF lymphoid enhancer factor, NR4A1 nuclear receptor subfamily 4 group A member 1, TEAD TEA domain family member, JAK Janus kinase, JNK c-Jun N-terminal kinase, SOCS3 suppressor of cytokine signaling 3, STAT3 signal transducer and activator of transcription 3. (The figure was generated with BioRender (https://biorender.com)
Fig. 4 Canonical signaling pathways involved in liver repair and regeneration. This diagram illustrates the key molecular components and regulatory mechanisms involved in different signaling pathways. RTK receptor tyrosine kinase, GPCR G-protein-coupled receptor, LGR leucine-rich repeat-containing G protein-coupled receptor, LRP low-density lipoprotein receptor-related protein, FZD frizzled, 5-HT 5-hydroxytryptamine. GLUT glucose transporter type, SMO smoothened, PTC patched, IL-6R, IL-6 receptor, gp130 glycoprotein 130, TNF-R, TNF receptor, TGFβ-R TGF-β receptor, PI3K phosphoinositide 3-kinase, AKT protein kinase B, mTORC1 mammalian target of rapamycin complex 1, WIP wild-type p53-induced phosphatase 1, S6K ribosomal S6 protein kinase, 4E-BP eukaryotic translation initiation factor 4E-binding protein, CXXC5 CXXC5-type zinc finger protein 5, DVL disheveled, ZNRF3, Zinc and Ring Finger 3, RNF43 Ring Finger Protein 43, TMEM9 transmembrane protein 9, APC adenomatous polyposis coli, GSK-3 glycogen synthase kinase 3, AXIN axis inhibition protein, CK1 casein kinase 1, AURKA aurora kinase A, MST ste20-like kinase, SAV salvador, LATS large tumor suppressor kinase, YAP Yes-associated protein, AMPK AMP-activated protein kinase, BRG1 brahma-related gene 1, CAR androstane receptor, PXR pregnane X receptor, PPARα peroxisome proliferator-activated receptor α, PFK1 phosphofructokinase-1, GLI zinc finger protein, SMAD suppressor of mothers against decapentaplegic, NOX4 NADPH oxidase 4, ROS reactive oxygen species, NICD Notch intracellular domain, TCF T-cell factor, LEF lymphoid enhancer factor, NR4A1 nuclear receptor subfamily 4 group A member 1, TEAD TEA domain family member, JAK Janus kinase, JNK c-Jun N-terminal kinase, SOCS3 suppressor of cytokine signaling 3, STAT3 signal transducer and activator of transcription 3. (The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 5 Glucose metabolism during liver repair and regeneration. A complex metabolic network regulates liver regeneration via gluconeogenesis, glycogen synthesis, and glycolysis. The arrows indicate upregulation or activation, and the T-arrows indicate downregulation or inhibition. AnxA6 annexin A6, AQP9 aquaporin-9, GLUT glucose transporter type, PEPCK phosphoenolpyruvate carboxykinase, GK glycerol kinase, GPD1 glycerol-3-phosphate dehydrogenase 1, GSK, glycogen synthase kinase, GS glycogen synthase, GCK glucokinase, PFK1 phosphofructokinase 1, PDK4 pyruvate dehydrogenase lipoamide kinase isozyme 4, PP2A, protein phosphatase 2, FOXM1, forkhead box protein M1, PFKFB2 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-2, FOXO1 forkhead box protein O1, HNF4α hepatocyte nuclear factor 4α, G6PC glucose-6-phosphatase catalytic subunit, PCK1 phosphoenolpyruvate carboxykinase 1, FASN fatty acid synthase, CPT1α carnitine palmitoyltransferase 1α, CDK5RAP3 Cyclin-dependent kinase 5 regulatory subunit associated protein 3. The figure was generated with BioRender (https://biorender.com)
Fig. 5 Glucose metabolism during liver repair and regeneration. A complex metabolic network regulates liver regeneration via gluconeogenesis, glycogen synthesis, and glycolysis. The arrows indicate upregulation or activation, and the T-arrows indicate downregulation or inhibition. AnxA6 annexin A6, AQP9 aquaporin-9, GLUT glucose transporter type, PEPCK phosphoenolpyruvate carboxykinase, GK glycerol kinase, GPD1 glycerol-3-phosphate dehydrogenase 1, GSK, glycogen synthase kinase, GS glycogen synthase, GCK glucokinase, PFK1 phosphofructokinase 1, PDK4 pyruvate dehydrogenase lipoamide kinase isozyme 4, PP2A, protein phosphatase 2, FOXM1, forkhead box protein M1, PFKFB2 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-2, FOXO1 forkhead box protein O1, HNF4α hepatocyte nuclear factor 4α, G6PC glucose-6-phosphatase catalytic subunit, PCK1 phosphoenolpyruvate carboxykinase 1, FASN fatty acid synthase, CPT1α carnitine palmitoyltransferase 1α, CDK5RAP3 Cyclin-dependent kinase 5 regulatory subunit associated protein 3. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 6 Lipid metabolism during liver repair and regeneration. Alterations in lipid metabolism during liver repair and regeneration. The arrows indicate upregulation or activation, and the T-arrows indicate downregulation or inhibition. TRAS transient regeneration-associated steatosis, TMA trimethylamine, TMAO trimethylamine N-oxide, FMO3 flavin-containing monooxygenase 3, BA bile acid, SCFA short-chain fatty acid, FGF fibroblast growth factor, FGFR4 fibroblast growth factor receptor 4, GLUT4 glucose transporter type 4, G6PD glucose-6-phosphate dehydrogenase, NADPH nicotinamide adenine dinucleotide phosphate, PPP pentose phosphate pathway, NCOR1 nuclear receptor corepressor 1, AMPK AMP-activated protein kinase, FASN fatty acid synthase, ACC acetyl-CoA carboxylase, SCD1 stearoyl-CoA desaturase 1, CPT1α carnitine palmitoyltransferase 1α, TEAD TEA domain family member, ZNRF3 Zinc and Ring Finger 3, RNF43 Ring Finger Protein 43, EGF epidermal growth factor, EGFR epidermal growth factor receptor, IL-6 interleukin-6, IL-6R, IL-6 receptor, VEGF vascular endothelial growth factor, MET mesenchymal-epithelial transition factor, HGF hepatocyte growth factor, SREBF1 sterol regulatory element-binding transcription factor 1, SPT serine palmitoyltransferase, ERRγ estrogen-related receptor γ, LOX lipoxygenase, COX cyclooxygenase, NRF2nuclear factor erythroid 2-related factor 2, ROS reactive oxygen species, LXRα liver X receptor α, TRIB1 tribbles homolog 1, MAGL monoacylglycerol lipase, PARK7 parkinsonism‐associated deglycase 7, PTEN phosphatase and tensin homolog, MIER1 mesoderm induction early response 1, EIF2S eukaryotic translation initiation factor 2 subunit, EET epoxyeicosatrienoic acid, TXA2 thromboxane A2, LTB4 leukotriene B4, PG prostaglandin, PGE2 prostaglandin E2, TRG5 G protein-coupled bile acid receptor 5, CYP cytochrome P450, NO nitric oxide, S1P sphingosine 1-phosphate, CYP7A1 cholesterol 7 alpha-hydroxylase, FXR farnesoid X receptor, HMGCR HMG-CoA reductase, INSIG2 insulin induced gene 2, SHP small heterodimer partner, GSK glycogen synthase kinase, GS glycogen synthase, FOXM1 forkhead box protein M1, PGC‐1α peroxisome proliferator‐activated receptor‐γ coactivator‐1α, PEPCK phosphoenolpyruvate carboxykinase, TLR Toll-like receptor, ABCA1 ATP-binding cassette transporter-A1, PPARα peroxisome proliferator-activated receptor α. The figure was generated with BioRender (https://biorender.com)
Fig. 6 Lipid metabolism during liver repair and regeneration. Alterations in lipid metabolism during liver repair and regeneration. The arrows indicate upregulation or activation, and the T-arrows indicate downregulation or inhibition. TRAS transient regeneration-associated steatosis, TMA trimethylamine, TMAO trimethylamine N-oxide, FMO3 flavin-containing monooxygenase 3, BA bile acid, SCFA short-chain fatty acid, FGF fibroblast growth factor, FGFR4 fibroblast growth factor receptor 4, GLUT4 glucose transporter type 4, G6PD glucose-6-phosphate dehydrogenase, NADPH nicotinamide adenine dinucleotide phosphate, PPP pentose phosphate pathway, NCOR1 nuclear receptor corepressor 1, AMPK AMP-activated protein kinase, FASN fatty acid synthase, ACC acetyl-CoA carboxylase, SCD1 stearoyl-CoA desaturase 1, CPT1α carnitine palmitoyltransferase 1α, TEAD TEA domain family member, ZNRF3 Zinc and Ring Finger 3, RNF43 Ring Finger Protein 43, EGF epidermal growth factor, EGFR epidermal growth factor receptor, IL-6 interleukin-6, IL-6R, IL-6 receptor, VEGF vascular endothelial growth factor, MET mesenchymal-epithelial transition factor, HGF hepatocyte growth factor, SREBF1 sterol regulatory element-binding transcription factor 1, SPT serine palmitoyltransferase, ERRγ estrogen-related receptor γ, LOX lipoxygenase, COX cyclooxygenase, NRF2nuclear factor erythroid 2-related factor 2, ROS reactive oxygen species, LXRα liver X receptor α, TRIB1 tribbles homolog 1, MAGL monoacylglycerol lipase, PARK7 parkinsonism‐associated deglycase 7, PTEN phosphatase and tensin homolog, MIER1 mesoderm induction early response 1, EIF2S eukaryotic translation initiation factor 2 subunit, EET epoxyeicosatrienoic acid, TXA2 thromboxane A2, LTB4 leukotriene B4, PG prostaglandin, PGE2 prostaglandin E2, TRG5 G protein-coupled bile acid receptor 5, CYP cytochrome P450, NO nitric oxide, S1P sphingosine 1-phosphate, CYP7A1 cholesterol 7 alpha-hydroxylase, FXR farnesoid X receptor, HMGCR HMG-CoA reductase, INSIG2 insulin induced gene 2, SHP small heterodimer partner, GSK glycogen synthase kinase, GS glycogen synthase, FOXM1 forkhead box protein M1, PGC‐1α peroxisome proliferator‐activated receptor‐γ coactivator‐1α, PEPCK phosphoenolpyruvate carboxykinase, TLR Toll-like receptor, ABCA1 ATP-binding cassette transporter-A1, PPARα peroxisome proliferator-activated receptor α. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 7 Amino acid metabolism during liver repair and regeneration. Amino acid metabolism involves multiple intracellular and extracellular pathways in different cell subsets. The arrows indicate upregulation or activation, and the T-arrows indicate downregulation or inhibition. TG2 transglutaminase 2, ADR adrenergic receptor, EGFR epidermal growth factor receptor, cAMP cyclic adenosine monophosphate, PKA protein kinase A, AC adenylate cyclase, HSL hormone-sensitive lipase, ATGL adipose triglyceride lipase, CPT1 carnitine palmitoyltransferase 1, TCA tricarboxylic acid, αKG α-ketoglutarate, GLS glutaminase, mTORC1 mammalian target of rapamycin complex 1, S6K1 S6 kinase 1, GCN5L1 general control of amino acid synthesis 5 like 1, FASN fatty acid synthase, FOXO1 forkhead box protein O1, AKT protein kinase B, PEPCK phosphoenolpyruvate carboxykinase, FBPase fructose bisphosphatase GP glycogen phosphorylase, G6P glucose 6-phosphate, G6Pase glucose 6-phosphatase. The figure was generated with BioRender (https://biorender.com)
Fig. 7 Amino acid metabolism during liver repair and regeneration. Amino acid metabolism involves multiple intracellular and extracellular pathways in different cell subsets. The arrows indicate upregulation or activation, and the T-arrows indicate downregulation or inhibition. TG2 transglutaminase 2, ADR adrenergic receptor, EGFR epidermal growth factor receptor, cAMP cyclic adenosine monophosphate, PKA protein kinase A, AC adenylate cyclase, HSL hormone-sensitive lipase, ATGL adipose triglyceride lipase, CPT1 carnitine palmitoyltransferase 1, TCA tricarboxylic acid, αKG α-ketoglutarate, GLS glutaminase, mTORC1 mammalian target of rapamycin complex 1, S6K1 S6 kinase 1, GCN5L1 general control of amino acid synthesis 5 like 1, FASN fatty acid synthase, FOXO1 forkhead box protein O1, AKT protein kinase B, PEPCK phosphoenolpyruvate carboxykinase, FBPase fructose bisphosphatase GP glycogen phosphorylase, G6P glucose 6-phosphate, G6Pase glucose 6-phosphatase. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 8 Overview of the molecular mechanisms affecting liver repair and regeneration under pathological conditions. This illustration shows the major pathophysiological mechanisms of various liver diseases and identifies molecular and signaling pathway targets with therapeutic potential. AILI acetaminophen-induced acute liver injury, NAFLD nonalcoholic fatty liver disease, NASH nonalcoholic steatohepatitis, ALD alcohol-related liver disease. The figure was generated with BioRender (https://biorender.com)
Fig. 8 Overview of the molecular mechanisms affecting liver repair and regeneration under pathological conditions. This illustration shows the major pathophysiological mechanisms of various liver diseases and identifies molecular and signaling pathway targets with therapeutic potential. AILI acetaminophen-induced acute liver injury, NAFLD nonalcoholic fatty liver disease, NASH nonalcoholic steatohepatitis, ALD alcohol-related liver disease. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central
Fig. 9 Innovations in analytical methods and therapeutic strategies. This illustration summarizes the characteristics of currently available treatment strategies and potential future treatments and highlights diagnostic approaches that can be used to explore new therapeutic targets. The figure was generated with BioRender (https://biorender.com)
Fig. 9 Innovations in analytical methods and therapeutic strategies. This illustration summarizes the characteristics of currently available treatment strategies and potential future treatments and highlights diagnostic approaches that can be used to explore new therapeutic targets. The figure was generated with BioRender (https://biorender.com)CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 1

  1. Higgins, G. M. & Anderson, R. M. Experimental pathology of the liver. I. Restoration of the liver of the white rat following partial surgical removal. Arch. Pathol. 12, 186–202 (1931).

Cited by

Sorted by citations

See all 134

Related

See all

Metadata

Authors
Ma, X., Huang, T., Chen, X., Li, Q., Liao, M., Fu, L., Huang, J., Yuan, K., Wang, Z., & Zeng, Y.
Affiliations
Sichuan University (CN)
Corresponding author
  • Wang, Zhen
  • Zeng, Yong
ORCID
Venue
Signal Transduction and Targeted Therapy
Publisher
Springer Science and Business Media LLC
Published
2025-02-08
Volume
10
Issue
1
Pages
63-63
ISSN
2059-3635 (ISSN-L)
DOI
10.1038/s41392-024-02104-8
PMC
PMC11806117
OpenAlex
W4407274978
Cited by
133
References
832
Citations by year
2026: 83 · 2025: 50
FWCI
19.43
Type
journal article
Language
en
Open access
Licence
Locations
  • Signal Transduction and Targeted Therapy (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (ZYJC18008, 82270643, 82170,621, 82070644)
  • Sichuan University (ZYJC18008)
  • West China Hospital, Sichuan University (ZYJC18008, ZYGD22006, 1.3.5)
Topics
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Surgery › Tissue Engineering and Regenerative Medicine
  • Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
Keywords
liver regeneration, liver repair, liver injury, liver microenvironment, cell-cell crosstalk, signaling pathways, metabolic reprogramming, glucose metabolism, lipid metabolism, amino acid metabolism, clinical trials
MeSH terms
Animals, Humans, Liver, Liver Diseases, Liver Regeneration, Signal Transduction

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review