Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (665 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Livers.
Where it fits in the MeSH classification
- Broader topics
- Digestive System
- Narrower topics
- Bile Ducts, Intrahepatic; Round Ligament of Liver
- See also
- Hepatectomy
Research landscape
PubMed indexes 504,144 records tagged with the MeSH heading “Liver” (counts retrieved 2026-10-31). 62,427 of them (12.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 277,988 records.
Reviews account for 32,732 records (6.5%) and meta-analyses for 1,047. Randomized controlled trials number 3,701 (0.7%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 277,988 |
| 2000-2009 | 72,181 |
| 2010-2019 | 91,548 |
| 2020 onward | 62,427 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 32,732 | 6.5% |
| Meta-analyses | 1,047 | 0.2% |
| Randomized controlled trials | 3,701 | 0.7% |
Method: PubMed query "Liver"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| TGF-β serves as a critical signaling determinant of liver progenitor cell activation and function | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42518287 · DOI · PMC13574154 |
| A Non-Canonical Role for Hepatocyte MLKL in Promoting Mitochondrial Dysfunction and Senescence in the Aging Liver | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42399678 · DOI · PMC13331751 |
| Enhanced Liver Fibrosis Test, FIB-4 and FibroScan: Real-World Prognostic Accuracy for MASLD in a Biopsy-Controlled Cohort | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42394207 · DOI · PMC13329087 |
TGF-β serves as a critical signaling determinant of liver progenitor cell activation and function [1]
Abstract reading summary — source excerpts
- Opening excerpt
- When massive hepatic necrosis-associated (MHN-associated) acute liver failure (ALF) occurs following severe damage, liver progenitor cells (LPCs) exit quiescence and enter differentiation programs during which they acquire hepatocyte-like functions.
- Closing excerpt
- These findings position TGF-β as a context-dependent determinant of LPC activation and lineage specification during ALF.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (202 words)
When massive hepatic necrosis-associated (MHN-associated) acute liver failure (ALF) occurs following severe damage, liver progenitor cells (LPCs) exit quiescence and enter differentiation programs during which they acquire hepatocyte-like functions. How LPCs maintain quiescence under physiological conditions and orchestrate activation following MHN remains largely unknown. We elucidate an essential role of TGF-β in regulating LPC quiescence and activation. Spatial transcriptomics and single-cell sequencing revealed that LPCs receive multiple signals, particularly TGF-β, HGF, and EGF, from surrounding hepatic stellate cells and macrophages in patients and zebrafish with MHN-induced ALF. Physiologically, TGF-β inhibits LPC proliferation by blocking G1-to-S phase transition, an effect reversed by Smad7 overexpression in a murine injury model. We observed extensive LPC proliferation in patients with ALF despite strong TGF-β/phosphorylated SMAD signaling. Immunostaining revealed concurrent activation of HGF/MET, EGF/EGFR, and downstream STAT3/ERK pathways in LPCs. In vitro, HGF or EGF overcame TGF-β-mediated growth arrest and promoted LPC proliferation. Beyond acting as a mitogen, HGF additionally induced hepatocyte gene programs (e.g., Hnf4a, Hnf1a) in LPCs. Strikingly, TGF-β signaling was required for HGF-dependent hepatocyte gene induction, indicating a dual role in restraining LPC proliferation and promoting functional maturation. These findings position TGF-β as a context-dependent determinant of LPC activation and lineage specification during ALF.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42518287 · DOI · PMC13574154
A Non-Canonical Role for Hepatocyte MLKL in Promoting Mitochondrial Dysfunction and Senescence in the Aging Liver [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Liver aging is characterized by chronic inflammation and metabolic dysfunction that drive progression of metabolic dysfunction-associated steatotic liver disease (MASLD).
- Closing excerpt
- Collectively, these findings reveal a non-lethal, non-necroptotic function of hepatocyte MLKL in promoting liver inflammaging via mitochondrial dysfunction and paracrine senescence signaling, identifying MLKL as a regulator of hepatic aging and a potential therapeutic target in age-associated liver disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (242 words)
Liver aging is characterized by chronic inflammation and metabolic dysfunction that drive progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Necroptosis, a pro-inflammatory form of cell death via the Receptor-Interacting serine/threonine-Protein Kinase 1 (RIPK1)-RIPK3-Mixed Lineage kinase domain Like pseudokinase (MLKL) pathway, is activated in aging livers, and systemic inhibition of this pathway reduces hepatic inflammation and pathology. The cell type-specific role of necroptosis in liver aging, however, is unclear. Notably, RIPK3 is suppressed in hepatocytes under metabolic disease, suggesting necroptosis independent functions for MLKL. Here, we show that MLKL is elevated in aged hepatocytes and drives liver aging via a non-necroptotic mechanism. Using hepatocyte-specific MLKL-overexpressing mice (MLKLHepOE), we find that MLKL overexpression does not induce necroptosis but instead promotes cellular senescence, evidenced by increased p16INK4a and p21WAF1/Cip1 and elevated senescence associated secretory phenotype (SASP). Mechanistically, MLKL induces hepatocyte mitochondrial dysfunction, with impaired respiration, altered mitochondrial dynamics, and increased reactive oxygen species, implicating oxidative stress as a contributing mechanism. This mitochondrial stress is associated with enhanced release of pro-inflammatory extracellular vesicles (EVs) and induction of senescence in hepatocytes and non-parenchymal cells. While hepatocytes contribute substantially to total senescent burden by abundance, macrophages emerge as a senescence-enriched population, indicating amplification of senescence through non-cell-autonomous signaling. Collectively, these findings reveal a non-lethal, non-necroptotic function of hepatocyte MLKL in promoting liver inflammaging via mitochondrial dysfunction and paracrine senescence signaling, identifying MLKL as a regulator of hepatic aging and a potential therapeutic target in age-associated liver disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42399678 · DOI · PMC13331751
Enhanced Liver Fibrosis Test, FIB-4 and FibroScan: Real-World Prognostic Accuracy for MASLD in a Biopsy-Controlled Cohort [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Background and aimsLiver fibrosis is a major determinant of liver-related events (LREs) in patients with metabolic dysfunction-associated steatotic liver disease (MASLD).
- Closing excerpt
- Larger prospective studies are needed to confirm these results and refine risk prediction strategies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (221 words)
Background and aimsLiver fibrosis is a major determinant of liver-related events (LREs) in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). Effective stratification based on fibrosis severity is essential for accurate prognosis. The Enhanced Liver Fibrosis (ELF) test, a non-invasive test measuring direct fibrosis markers, offers a potential alternative to traditional methods like FIB-4, liver stiffness measurement (LSM) and liver biopsy. This study aims to evaluate the prognostic value of the ELF test in comparison with these established methods.MethodsWe retrospectively analysed 289 MASLD patients (30.4% female, median age 49 years [IQR 39-58], 28% with type 2 diabetes) from the PROMETEO cohort (NCT04371042). We excluded patients with prior or current evidence of decompensated cirrhosis. At baseline, patients underwent liver biopsy, FIB-4, ELF and LSM assessments. The primary outcome was development of Liver Related Events (LRE), a composite of liver-related death, hepatocellular carcinoma, liver transplantation, ascites, encephalopathy or variceal bleeding.ResultsOver a median follow-up of 64 months [IQR 39-81], 41 patients (14.2%) experienced LREs. Event rates increased markedly across ELF categories (1% for ELF ConclusionsIn this biopsy-proven MASLD cohort, ELF provided prognostic stratification for liver-related events comparable to liver histology and LSM. Given the limited number of outcome events, these findings support the non-inferiority of ELF rather than definitive superiority. Larger prospective studies are needed to confirm these results and refine risk prediction strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42394207 · DOI · PMC13329087
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: Systematic review and meta-analysis [4]
- Research article Association Between Fibrosis Stage and Outcomes of Patients With Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis [5]
- Research article Comparison of laboratory tests, ultrasound, or magnetic resonance elastography to detect fibrosis in patients with nonalcoholic fatty liver disease: A meta-analysis [6]
- Research article Treatment and Prognosis for Patients With Intrahepatic Cholangiocarcinoma: Systematic Review and Meta-analysis [7]
- Research article Genomic and genetic characterization of cholangiocarcinoma identifies therapeutic targets for tyrosine kinase inhibitors [8]
- Research article Diagnostic performance of magnetic resonance elastography in staging liver fibrosis: a systematic review and meta-analysis of individual participant data [9]
References
- Tong C, Lin T, Wang H, Jiang L, Yuan X, Luo W, et al.. TGF-β serves as a critical signaling determinant of liver progenitor cell activation and function. . 2026. PMID 42518287 · DOI · PMC13574154
- Mohammed S, Jiang C, Pennington T, Bhaskaran S, Ohene-Marfo P, Kneuper KF, et al.. A Non-Canonical Role for Hepatocyte MLKL in Promoting Mitochondrial Dysfunction and Senescence in the Aging Liver. . 2026. PMID 42399678 · DOI · PMC13331751
- Liguori A, D'Ambrosio F, Angelini G, Cefalo C, Galletti S, Cardinali S, et al.. Enhanced Liver Fibrosis Test, FIB-4 and FibroScan: Real-World Prognostic Accuracy for MASLD in a Biopsy-Controlled Cohort. . 2026. PMID 42394207 · DOI · PMC13329087
- Dulai PS, Singh S, Patel J, Soni M, Prokop LJ, Younossi Z, et al.. Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: Systematic review and meta-analysis. Hepatology. 2017. PMID 28130788 · DOI · PMC5397356
- Taylor RS, Taylor RJ, Bayliss S, Hagström H, Nasr P, Schattenberg JM, et al.. Association Between Fibrosis Stage and Outcomes of Patients With Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis. Gastroenterology. 2020. PMID 32027911 · DOI
- Xiao G, Zhu S, Xiao X, Yan L, Yang J, Wu G. Comparison of laboratory tests, ultrasound, or magnetic resonance elastography to detect fibrosis in patients with nonalcoholic fatty liver disease: A meta-analysis. Hepatology. 2017. PMID 28586172 · DOI
- Mavros MN, Economopoulos KP, Alexiou VG, Pawlik TM. Treatment and Prognosis for Patients With Intrahepatic Cholangiocarcinoma: Systematic Review and Meta-analysis. JAMA Surg. 2014. PMID 24718873 · DOI
- Andersen JB, Spee B, Blechacz BR, Avital I, Komuta M, Barbour A, et al.. Genomic and genetic characterization of cholangiocarcinoma identifies therapeutic targets for tyrosine kinase inhibitors. Gastroenterology. 2012. PMID 22178589 · DOI · PMC3413201
- Singh S, Venkatesh SK, Wang Z, Miller FH, Motosugi U, Low RN, et al.. Diagnostic performance of magnetic resonance elastography in staging liver fibrosis: a systematic review and meta-analysis of individual participant data. Clin Gastroenterol Hepatol. 2015. PMID 25305349 · DOI · PMC4333001
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.