Evidence map›Paper›PMID 18336657›Full record

ReviewJournal of gastroenterology and hepatology2008

Dissection of endoplasmic reticulum stress signaling in alcoholic and non-alcoholic liver injury.

Cheng Ji

Open access · greenAbstract readReview
In one paragraph

Review in Journal of gastroenterology and hepatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 132 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Endoplasmic reticulum stress and liver diseases.Liver research (Beijing, China) · 2019
    Article
  17. Role and mechanisms of autophagy in alcohol-induced liver injury.Advances in pharmacology (San Diego, Calif.) · 2019
    Review
  18. Article
  19. [Effects of sera of rats fed withNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  20. Article

12 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

1 author at 1 institution in 1 country.

Cheng JiUSC-UCLA Research Center for Alcoholic Liver and Pancreatic Diseases, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA. chengji@usc.edu
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
Homocysteine, ER Stress and Alcoholic Liver Injury.R01AA014428 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JI, CHENG, KAPLOWITZ, NEIL · 2004 to 2014
$3.7M
NIAAA NIH HHS P50 AA011999NIAAA NIH HHS P50 AA11999NIAAA NIH HHS R01 AA014428NIDDK NIH HHS P30 DK048522NIDDK NIH HHS P30 DK48522
6 · The paper itself

Abstract

Accumulation of unfolded or malfolded proteins induces endoplasmic reticulum (ER) stress which elicits a complex network of interacting and parallel responses that dampen the stress. The ER stress response in the liver is controlled by intrinsic feedback effectors and is initially protective. However, delayed or insufficient responses or interplay with mitochondrial dysfunction may turn physiological mechanisms into pathological consequences including apoptosis, fat accumulation and inflammation all of which have an important role in the pathogenesis of liver disorders such as genetic mutations, viral hepatitis, insulin resistance, ischemia/reperfusion injury, and alcoholic and non-alcoholic steatosis. In both alcohol and non-alcohol-induced ER stress, a common candidate is hyperhomocysteinemia. Betaine supplementation and/or expression of betaine-homocysteine methyltransferase (BHMT) promote removal of homocysteine and alleviate ER stress, fatty accumulation and apoptosis in cultured hepatocytes and mouse models. The rapidity and magnitude of homocysteine-induced activation of each of the main ER resident transmembrane sensors including inositol requiring enzyme 1 (IRE-l alpha), activating transcription factor 6 (ATF-6) and RNA-activated protein kinase (PKR)-like ER kinase (PERK) appear different in different experimental models. Dissection and differentiation of ER stress signaling may reveal clues on the specific importance of the ER stress response in contributing to liver injury and thus provide better strategies on prevention and treatment of liver disease.

Indexed as

Diabetes ComplicationsEndoplasmic ReticulumFatty LiverHumansHyperhomocysteinemiaLiver DiseasesLiver Diseases, AlcoholicSignal Transduction

Identifiers

PMID18336657
PMCPMC2491335
OpenAlexW2064820279

What OpenQuestion holds

Textmetadata
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.