Evidence map›Paper›PMID 21384408›Full record

ArticleHepatology (Baltimore, Md.)2011

The contribution of endoplasmic reticulum stress to liver diseases.

Lily Dara, Cheng Ji, Neil Kaplowitz

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
10.2field-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

180 citing papers in PubMed, 372 citations in OpenAlex.

  1. Article
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  6. Review
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  10. Review
  11. [Vitexin-4 ″-Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Roles of X-box binding protein 1 in liver pathogenesis.Clinical and molecular hepatology · 2025
    Review
  16. Article
  17. Observational
  18. Article
  19. Article
  20. Article

120 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 1 institution in 1 country.

Lily DaraUniversity of Southern California Research Center for Liver Diseases, Los Angeles, CA, USA. lily.dara@usc.edu
Cheng Ji
Neil Kaplowitz
University of Southern California · US

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
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
Role of aberrant regulation of organelle stress responses in alcohol-induced liveR01AA018846 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JI, CHENG · 2009 to 2012
$1.5M
Effect of HIV protease inhibitor on alcohol induced ER stress and liver injury.R01AA018612 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JI, CHENG · 2010 to 2013
$1.5M
NIAAA NIH HHS P50 AA011999NIAAA NIH HHS P50 AA11999NIAAA NIH HHS R01 AA014428NIAAA NIH HHS R01 AA018612NIAAA NIH HHS R01 AA018846NIDDK NIH HHS P30 DK048522NIDDK NIH HHS P30 DK48522NIDDK NIH HHS R01 DK067215NIDDK NIH HHS R01DK067215
6 · The paper itself

Abstract

The unfolded protein response (UPR) is an evolutionarily conserved cell signaling pathway that is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed from increased client protein load or the accumulation of unfolded or malfolded proteins. Once activated, this signaling pathway can either result in the recovery of homeostasis or can activate a cascade of events that ultimately result in cell death. The UPR/endoplasmic reticulum (ER) stress response spectrum and its interplay with other cellular organelles play an important role in the pathogenesis of disease in secretory cells rich in ER, such as hepatocytes. Over the past 2 decades, the contribution of ER stress to various forms of liver diseases has been examined. Robust support for a contributing, as opposed to a secondary role, for ER stress response is seen in the nonalcoholic steatohepatitis, alcoholic liver disease, ischemia/reperfusion injury, and cholestatic models of liver disease. The exact direction of the cause and effect relationship between modes of cell injury and ER stress remains elusive. It is apparent that a complex interplay exists between ER stress response, conditions that promote it, and those that result from it. A vicious cycle in which ER stress promotes inflammation, cell injury, and steatosis and in which steatogenesis, inflammation, and cell injury aggravate ER stress seems to be at play. It is perhaps the nature of such a vicious cycle that is the key pathophysiologic concept. Therapeutic approaches aimed at interrupting the cycle may dampen the stress response and the ensuing injury.

Indexed as

Stress, PhysiologicalUnfolded Protein ResponseAnimalsChemical and Drug Induced Liver InjuryEndoplasmic ReticulumFatty LiverHepatitis, Viral, HumanHumansHyperhomocysteinemiaLiver DiseasesLiver Diseases, Alcoholic

Identifiers

PMID21384408
PMCPMC3082587
OpenAlexW1966625828

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.