Evidence map›Paper›PMID 23720337›Full record

ReviewComprehensive Physiology2013

Apoptosis and necrosis in the liver.

Maria Eugenia Guicciardi, Harmeet Malhi, Justin L Mott, Gregory J Gores

Abstract readReview
In one paragraph

Review in Comprehensive Physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

183 citing papers in PubMed, 1 synthesis or guideline pooled it, 360 citations in OpenAlex.

  1. Regional Citrate Anticoagulation or Heparin Anticoagulation for Renal Replacement Therapy in Patients With Liver Failure: A Systematic Review and Meta-Analysis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Pooled it
  2. Review
  3. [IOX1 alleviates hepatic ischemia-reperfusion injury by inhibiting mitogen-activated protein kinase signaling pathway].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Article
  4. Article
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  7. Review
  8. Article
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  10. Review
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  13. Review
  14. Xingkai Lake Topmouth Culter (Antioxidants (Basel, Switzerland) · 2025
    Article
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  17. Review
  18. Article
  19. Article
  20. Article

123 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

4 authors at 2 institutions in 1 country.

Maria Eugenia Guicciardi1Division of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Harmeet Malhi
Justin L Mott
Gregory J Gores
Mayo Clinic · USUniversity of Nebraska Medical Center · US

Funding

Organelle Dysfunction and Apoptosis in Liver EpitheliaR01DK063947 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2003 to 2016
$4.1M
MECHANISMS OF LIVER CELL INJURYR01DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 1992 to 2019
$3.6M
MECHANISMS OF LIVER CELL INJURYR37DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2000 to 2009
$2.9M
Apoptosis Effectors Targeted By Hedgehog-Supported MicroRNAsR03DK092263 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MOTT, JUSTIN L. · 2011 to 2012
$149k
NIDDK NIH HHS R01 DK041876NIDDK NIH HHS R01 DK063947NIDDK NIH HHS R01 DK41876NIDDK NIH HHS R01 DK63947NIDDK NIH HHS R03 DK092263NIDDK NIH HHS R37 DK041876
6 · The paper itself

Abstract

Because of its unique function and anatomical location, the liver is exposed to a multitude of toxins and xenobiotics, including medications and alcohol, as well as to infection by hepatotropic viruses, and therefore, is highly susceptible to tissue injury. Cell death in the liver occurs mainly by apoptosis or necrosis, with apoptosis also being the physiologic route to eliminate damaged or infected cells and to maintain tissue homeostasis. Liver cells, especially hepatocytes and cholangiocytes, are particularly susceptible to death receptor-mediated apoptosis, given the ubiquitous expression of the death receptors in the organ. In a quite unique way, death receptor-induced apoptosis in these cells is mediated by both mitochondrial and lysosomal permeabilization. Signaling between the endoplasmic reticulum and the mitochondria promotes hepatocyte apoptosis in response to excessive free fatty acid generation during the metabolic syndrome. These cell death pathways are partially regulated by microRNAs. Necrosis in the liver is generally associated with acute injury (i.e., ischemia/reperfusion injury) and has been long considered an unregulated process. Recently, a new form of "programmed" necrosis (named necroptosis) has been described: the role of necroptosis in the liver has yet to be explored. However, the minimal expression of a key player in this process in the liver suggests this form of cell death may be uncommon in liver diseases. Because apoptosis is a key feature of so many diseases of the liver, therapeutic modulation of liver cell death holds promise. An updated overview of these concepts is given in this article.

Indexed as

ApoptosisAnimalsHepatocytesHumansLiverNecrosis

Identifiers

PMID23720337
PMCPMC3867948
OpenAlexW1559041257

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.