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 (488 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 group of organs stretching from the mouth to the ANUS, serving to breakdown foods, assimilate nutrients, and eliminate waste. In humans, the digestive system includes the gastrointestinal tract and the accessory glands (liver; biliary tract; pancreas).
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: Ailmentary System; Alimentary System.
Where it fits in the MeSH classification
- Broader topics
- Anatomy Category
- Narrower topics
- Biliary Tract; Gastrointestinal Tract; Liver; Pancreas
Related concepts
- Mouth
- Gastrointestinal Tract
- Liver
- Biliary Tract
- Pancreas
Research landscape
PubMed indexes 1,380,888 records tagged with the MeSH heading “Digestive System” (counts retrieved 2026-10-31). 169,661 of them (12.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 720,111 records.
Reviews account for 109,496 records (7.9%) and meta-analyses for 4,321. Randomized controlled trials number 17,676 (1.3%) 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 | 720,111 |
| 2000-2009 | 215,004 |
| 2010-2019 | 276,112 |
| 2020 onward | 169,661 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 109,496 | 7.9% |
| Meta-analyses | 4,321 | 0.3% |
| Randomized controlled trials | 17,676 | 1.3% |
Method: PubMed query "Digestive System"[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 |
|---|---|---|---|---|
| Ninjurin-1 mediates hepatic ischemia-reperfusion injury | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42647649 · DOI · PMC13510749 |
| Impaired liver-muscle lactate metabolism causes sarcopenia via lactic acidosis in skeletal muscle in mice | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42696581 · DOI · PMC13544239 |
| SETD6-mediated methylation of PPARγ establishes a transcriptional feedback circuit promoting lipid accumulation in liver-derived cells | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42663329 · DOI · PMC13524377 |
Ninjurin-1 mediates hepatic ischemia-reperfusion injury [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Lytic cell death pathways drive hepatic ischemia-reperfusion injury (IRI).
- Closing excerpt
- We therefore position NINJ1 as a potential new therapeutic target to limit hepatic IRI, with important implications for liver transplantation.
- 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 (157 words)
Lytic cell death pathways drive hepatic ischemia-reperfusion injury (IRI). The transmembrane protein ninjurin-1 (NINJ1) aggregates in the plasma membrane to permeabilize the cell during multiple cell death pathways implicated in hepatic IRI. We hypothesized that NINJ1 mediates liver IRI and that its inhibition would mitigate injury. We found that NINJ1 is highly expressed in human liver tissue and that its up-regulation and activation correlate with early allograft dysfunction in liver transplant patients. Using a segmental hepatic IRI model in mice and rats, Ninj1 genetic deletion or pharmacologic inhibition diminished acute injury. Mice with hepatocyte- or macrophage-specific Ninj1 knockout had reduced hepatocellular injury following IRI, suggesting that NINJ1 within both populations contributes to the resulting liver injury. Mechanistically, we found that hepatocytes and Kupffer cells are susceptible to hypoxia-induced NINJ1-mediated plasma membrane rupture, which can be pharmacologically prevented. We therefore position NINJ1 as a potential new therapeutic target to limit hepatic IRI, with important implications for liver transplantation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42647649 · DOI · PMC13510749
Impaired liver-muscle lactate metabolism causes sarcopenia via lactic acidosis in skeletal muscle in mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Sarcopenia is a progressive disease characterized by age-related decline in skeletal muscle force and mass.
- Closing excerpt
- Using mouse models, our results show lactic acidosis in skeletal muscle as a key molecular pathogenesis of sarcopenia and highlight HIF1α in the liver as a pharmacological target for sarcopenia.
- 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 (153 words)
Sarcopenia is a progressive disease characterized by age-related decline in skeletal muscle force and mass. The fundamental molecular pathogenesis of sarcopenia has not yet been elucidated. Here, we show that the accumulation of lactate and intracellular acidification, lactic acidosis, in skeletal muscle owing to impaired liver-skeletal muscle lactate metabolism is the fundamental cause of sarcopenia. Systemic lactate tolerance decreased in aged mice owing to the impaired lactate processing capacity in the liver, which caused lactic acidosis in skeletal muscle. Furthermore, pharmacological activation of hypoxia-inducible factor (HIF) or liver-specific activation of HIF1α improved age-associated impairment in lactate tolerance, lactic acidosis in skeletal muscle, and sarcopenia. Mechanistically, the decreased nicotinamide adenine dinucleotide level was the cause of dysregulated skeletal muscle functions due to lactic acidosis. Using mouse models, our results show lactic acidosis in skeletal muscle as a key molecular pathogenesis of sarcopenia and highlight HIF1α in the liver as a pharmacological target for sarcopenia.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42696581 · DOI · PMC13544239
SETD6-mediated methylation of PPARγ establishes a transcriptional feedback circuit promoting lipid accumulation in liver-derived cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Peroxisome proliferator-activated receptor gamma (PPARγ) is a key transcriptional regulator of genes mediating adipogenesis (fat-cell differentiation), and lipid storage in several cell types like hepatocytes.
- Closing excerpt
- Together, our findings uncover a novel role for lysine methylation of PPARγ in the regulation of lipid synthesis and lipid droplet biogenesis, thereby identifying putative new therapeutic targets for lipid overproduction diseases, including metabolic dysfunction-associated fatty liver disease and obesity.
- 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 (178 words)
Peroxisome proliferator-activated receptor gamma (PPARγ) is a key transcriptional regulator of genes mediating adipogenesis (fat-cell differentiation), and lipid storage in several cell types like hepatocytes. As such, its regulation is crucial for cell and organismal physiology. Indeed, PPARγ's activity is regulated by multiple mechanisms, including post-transcriptional modifications, which, when dys-coordinated, may contribute to the pathogenesis of various states, including obesity, insulin resistance, and fatty liver disease. Here, we demonstrate that SETD6 binds to and methylates PPARγ at lysine 170 (K170) both in vitro and in liver-derived cells. This methylation event, in turn, is required for PPARγ-mediated activation of SETD6 transcription via promoter binding, forming a positive feedback regulatory loop. RNA-sequencing revealed that both SETD6 and PPARγ methylation at K170 are required for full induction of lipid metabolism genes' expression, manifesting functionally in lipid droplet biogenesis in liver-derived cells. Together, our findings uncover a novel role for lysine methylation of PPARγ in the regulation of lipid synthesis and lipid droplet biogenesis, thereby identifying putative new therapeutic targets for lipid overproduction diseases, including metabolic dysfunction-associated fatty liver disease and obesity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42663329 · DOI · PMC13524377
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 Streptococcus mutans and Caries: A Systematic Review and Meta-Analysis [4]
- Research article Can artificial intelligence replace endoscopists when assessing mucosal healing in ulcerative colitis? A systematic review and diagnostic test accuracy meta-analysis [5]
- Research article Liver eQTL meta-analysis illuminates potential molecular mechanisms of cardiometabolic traits [6]
- Research article The effect of synbiotics on liver enzymes, obesity indices, blood pressure, lipid profile, and inflammation in patients with non-alcoholic fatty liver: A systematic review and meta-analysis of randomized controlled trials [7]
- Research article A systematic review and meta-analysis of randomized controlled trials: effects of mediterranean diet and low-fat diet on liver enzymes and liver fat content of NAFLD [8]
- Research article The efficacy and safety of PD-1/PD-L1 inhibitors in combination with chemotherapy as a first-line treatment for unresectable, locally advanced, HER2-negative gastric or gastroesophageal junction cancer: a meta-analysis of randomized controlled trials [9]
References
- Mossemann J, Martins BX, Zhao Y, Aguilar F, Taskina D, Hur CJ, et al.. Ninjurin-1 mediates hepatic ischemia-reperfusion injury. . 2026. PMID 42647649 · DOI · PMC13510749
- Eguchi T, Hayashiji N, Tabata S, Kabetani K, Shintani Y, Makinoshima H, et al.. Impaired liver-muscle lactate metabolism causes sarcopenia via lactic acidosis in skeletal muscle in mice. . 2026. PMID 42696581 · DOI · PMC13544239
- Nashnaz N, Goldberg D, Abramov M, Chopra A, Rosiecki T, Muallem H, et al.. SETD6-mediated methylation of PPARγ establishes a transcriptional feedback circuit promoting lipid accumulation in liver-derived cells. . 2026. PMID 42663329 · DOI · PMC13524377
- Mazurel D, Brandt BW, Boomsma M, Crielaard W, Lagerweij M, Exterkate RAM, et al.. Streptococcus mutans and Caries: A Systematic Review and Meta-Analysis. J Dent Res. 2025. PMID 39895020 · DOI · PMC12075887
- Rimondi A, Gottlieb K, Despott EJ, Iacucci M, Murino A, Tontini GE. Can artificial intelligence replace endoscopists when assessing mucosal healing in ulcerative colitis? A systematic review and diagnostic test accuracy meta-analysis. Dig Liver Dis. 2024. PMID 38057218 · DOI
- Broadaway KA, Brotman SM, Rosen JD, Currin KW, Alkhawaja AA, Etheridge AS, et al.. Liver eQTL meta-analysis illuminates potential molecular mechanisms of cardiometabolic traits. Am J Hum Genet. 2024. PMID 39173627 · DOI · PMC11393674
- Musazadeh V, Assadian K, Rajabi F, Faghfouri AH, Soleymani Y, Kavyani Z, et al.. The effect of synbiotics on liver enzymes, obesity indices, blood pressure, lipid profile, and inflammation in patients with non-alcoholic fatty liver: A systematic review and meta-analysis of randomized controlled trials. Pharmacol Res. 2024. PMID 39241935 · DOI
- Xiong Y, Shi X, Xiong X, Li S, Zhao H, Song H, et al.. A systematic review and meta-analysis of randomized controlled trials: effects of mediterranean diet and low-fat diet on liver enzymes and liver fat content of NAFLD. Food Funct. 2024. PMID 39076035 · DOI
- Pu W, Li S, Zhang J, Huang J, Li J, Jiang Y, et al.. The efficacy and safety of PD-1/PD-L1 inhibitors in combination with chemotherapy as a first-line treatment for unresectable, locally advanced, HER2-negative gastric or gastroesophageal junction cancer: a meta-analysis of randomized controlled trials. Front Immunol. 2025. PMID 40207218 · DOI · PMC11979168
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.