Evidence map›Paper›PMID 25046161›Full record

ReviewGastroenterology2014

Cell death and cell death responses in liver disease: mechanisms and clinical relevance.

Tom Luedde, Neil Kaplowitz, Robert F Schwabe

Open access · bronzeAbstract readReview
In one paragraph

Review in Gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 397 papers.

0numbers the graph read from it
0cells of the map it votes in
397citing papers in PubMed
33.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

397 citing papers in PubMed, 733 citations in OpenAlex.

  1. Article
  2. Article
  3. Ferroptosis in liver biology and diseases.Hepatology communications · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. ALDH2 Mediated Ferroptosis Regulation in Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Exercise Impacts Liver Disease: Balancing Metabolic and Immune Homeostasis.International journal of biological sciences · 2026
    Review
  17. Review
  18. Review
  19. Review
  20. Article

337 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Tom LueddeDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, Germany. Electronic address: tluedde@ukaachen.de.
Neil KaplowitzDivision of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, California.
Robert F SchwabeDepartment of Medicine, Columbia University, New York, New York; Institute of Human Nutrition, Columbia University, New York, New York. Electronic address: rfs2102@cumc.columbia.edu.
Columbia University · USRWTH Aachen University · DEUniversity of Southern California · US

Funding

Role of Glutathione Redox Status in HepatotoxicityR01DK067215 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 2005 to 2019
$5.6M
Homocysteine, ER Stress and Alcoholic Liver Injury.R01AA014428 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JI, CHENG, KAPLOWITZ, NEIL · 2004 to 2014
$3.7M
Targeting Cancer-Associated Myofibroblasts by DNA HypomethylationU54CA163111 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI WANG, TIMOTHY CRAGIN · 2011 to 2015
$2.6M
Role of the Gut Microbiota and TLR4 in Alcoholic HepatocarcinogenesisR01AA020211 · NIAAA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SCHWABE, ROBERT F. · 2010 to 2014
$2.0M
Targeting DAMPs in Alcoholic HepatitisU01AA021912 · NIAAA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MEHAL, WAJAHAT ZAFAR, SCHWABE, ROBERT F. · 2013 to 2017
$1.9M
European Research Council 208237NCI NIH HHS 5U54CA163111NCI NIH HHS U54 CA163111NIAAA NIH HHS 1U01AA021912NIAAA NIH HHS 5R01AA014428NIAAA NIH HHS 5R01AA020211NIAAA NIH HHS R01 AA020211NIAAA NIH HHS U01 AA021912NIDDK NIH HHS 5P30DK0485NIDDK NIH HHS 5R01DK067215
6 · The paper itself

Abstract

Hepatocellular death is present in almost all types of human liver disease and is used as a sensitive parameter for the detection of acute and chronic liver disease of viral, toxic, metabolic, or autoimmune origin. Clinical data and animal models suggest that hepatocyte death is the key trigger of liver disease progression, manifested by the subsequent development of inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. Modes of hepatocellular death differ substantially between liver diseases. Different modes of cell death such as apoptosis, necrosis, and necroptosis trigger specific cell death responses and promote progression of liver disease through distinct mechanisms. In this review, we first discuss molecular mechanisms by which different modes of cell death, damage-associated molecular patterns, and specific cell death responses contribute to the development of liver disease. We then review the clinical relevance of cell death, focusing on biomarkers; the contribution of cell death to drug-induced, viral, and fatty liver disease and liver cancer; and evidence for cell death pathways as therapeutic targets.

Indexed as

ApoptosisAnimalsBiomarkersHepatocytesHumansLiverLiver DiseasesNecrosisSignal TransductionBiomarkersAlcoholic Liver DiseaseApoptosisCaspasesClinical TrialDAMPDILIHepatocellular CarcinomaNASHNecroptosisNecrosisNecrosomeRIP3RIP KinasesViral Hepatitis

Identifiers

PMID25046161
PMCPMC4531834
OpenAlexW2142225943

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.