Evidence map›Paper›PMID 27516341›Full record

ReviewNature reviews. Endocrinology2016

Endoplasmic reticulum proteostasis in hepatic steatosis.

Andrei Baiceanu, Pierre Mesdom, Marie Lagouge, Fabienne Foufelle

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
13.6field-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

103 citing papers in PubMed, 206 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The E3 Ligase RNF8 Promotes Ubiquitination and Degradation of ChREBPα During Liver Stress Response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

43 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.

Andrei BaiceanuInstitut National de la Santé et de la Recherche Médicale, UMRS 1138, Centre de Recherche des Cordeliers, F-75006, Paris, France.
Pierre MesdomInstitut National de la Santé et de la Recherche Médicale, UMRS 1138, Centre de Recherche des Cordeliers, F-75006, Paris, France.
Marie LagougeInstitut National de la Santé et de la Recherche Médicale, UMRS 1138, Centre de Recherche des Cordeliers, F-75006, Paris, France.
Fabienne FoufelleInstitut National de la Santé et de la Recherche Médicale, UMRS 1138, Centre de Recherche des Cordeliers, F-75006, Paris, France.
Centre de Recherche des Cordeliers · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic steatosis, the first step in the progression of nonalcoholic fatty liver disease, is characterized by triglyceride accumulation in hepatocytes and is highly prevalent in people with obesity. Although initially asymptomatic, hepatic steatosis is an important risk factor for the development of hepatic insulin resistance and type 2 diabetes mellitus and can also progress to more severe pathologies such as nonalcoholic steatohepatitis, liver fibrosis and cirrhosis; hepatic steatosis has, therefore, received considerable research interest in the past 20 years. The lipid accumulation that defines hepatic steatosis disturbs the function of the endoplasmic reticulum (ER) in hepatocytes, thereby generating chronic ER stress that interferes with normal cellular function. Although ubiquitous stress response mechanisms (namely, ER-associated degradation, unfolded protein response and autophagy) are the main processes for restoring cellular proteostasis, these mechanisms are unable to alleviate ER stress in the context of the fatty liver. Furthermore, ER stress and ER stress responses can promote lipid accumulation in hepatocytes in a counter-productive manner and could, therefore, be the origin of a vicious pathological cycle.

Indexed as

AutophagyEndoplasmic Reticulum-Associated DegradationEndoplasmic Reticulum StressLipid MetabolismUnfolded Protein ResponseDiabetes Mellitus, Type 2Endoplasmic ReticulumFatty LiverHepatocytesHomeostasisHumansInsulin ResistanceLiverObesityOrganellesProteinsProteinsTriglycerides

Identifiers

PMID27516341
OpenAlexW2513893629

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.