Evidence map›Paper›PMID 27146479›Full record

ReviewJournal of lipid research2016

The role of ER stress in lipid metabolism and lipotoxicity.

Jaeseok Han, Randal J Kaufman

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 357 papers.

0numbers the graph read from it
0cells of the map it votes in
357citing papers in PubMed
22.5field-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

357 citing papers in PubMed, 639 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Antioxidants (Basel, Switzerland) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Treatment with saponins fromNutrition research and practice · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

297 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

2 authors at 2 institutions in 2 countries.

Jaeseok HanSoonchunhyang Institute of Med-bio Science (SIMS), Soonchunhyang University, Cheonan-si, Choongchungnam-do, 31151, Republic of Korea hanjs015@sch.ac.kr rkaufman@sbpdiscovery.org.
Randal J KaufmanDegenerative Diseases Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92307 hanjs015@sch.ac.kr rkaufman@sbpdiscovery.org.
Sanford Burnham Prebys Medical Discovery Institute · USSoonchunhyang University · KR

Funding

Tumor Assessment CoreP01CA128814 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI SMITH, JEFFREY W · 2009 to 2020
$19.1M
Role of the Unfolded Protein Response in Beta CellR37DK042394 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAUFMAN, RANDAL J. · 2007 to 2016
$4.9M
Regulation of ER stress-induced cell deathR01DK088227 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAUFMAN, RANDAL J. · 2010 to 2014
$3.1M
Unfolded Protein Response in Glucose HomeostasisR01DK042394 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAUFMAN, RANDAL J. · 2003 to 2006
$1.2M
Streamlined Diagnostic Strategy for Primary AldosteronismR21DK103183 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI AUCHUS, RICHARD J., RAINEY, WILLIAM E · 2015 to 2016
$426k
NCI NIH HHS P01 CA128814NIDDK NIH HHS R01 DK042394NIDDK NIH HHS R01 DK088227NIDDK NIH HHS R21 DK103183NIDDK NIH HHS R37 DK042394
6 · The paper itself

Abstract

The endoplasmic reticulum (ER) is a cellular organelle important for regulating calcium homeostasis, lipid metabolism, protein synthesis, and posttranslational modification and trafficking. Numerous environmental, physiological, and pathological insults disturb ER homeostasis, referred to as ER stress, in which a collection of conserved intracellular signaling pathways, termed the unfolded protein response (UPR), are activated to maintain ER function for cell survival. However, excessive and/or prolonged UPR activation leads to initiation of self-destruction through apoptosis. Excessive accumulation of lipids and their intermediate products causes metabolic abnormalities and cell death, called lipotoxicity, in peripheral organs, including the pancreatic islets, liver, muscle, and heart. Because accumulating evidence links chronic ER stress and defects in UPR signaling to lipotoxicity in peripheral tissues, understanding the role of ER stress in cell physiology is a topic under intense investigation. In this review, we highlight recent findings that link ER stress and UPR signaling to the pathogenesis of peripheral organs due to lipotoxicity.

Indexed as

Endoplasmic Reticulum StressLipid MetabolismAnimalsApoptosisEndoplasmic ReticulumHumansLiverMuscle, SkeletalMyocardiumUnfolded Protein Responsecell signalingdiabetesendoplasmic reticulumfatty acidlipids

Identifiers

PMID27146479
PMCPMC4959874
OpenAlexW2345368448

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.