Evidence map›Paper›PMID 16319173›Full record

ArticleMolecular biology of the cell2006

A critical role for eukaryotic elongation factor 1A-1 in lipotoxic cell death.

Nica M Borradaile, Kimberly K Buhman, Laura L Listenberger, Carolyn J Magee, Emiko T A Morimoto, Daniel S Ory, Jean E Schaffer

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

75 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Current Perspectives of Mitochondria in Sepsis-Induced Cardiomyopathy.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
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  8. Review
  9. Article
  10. Review
  11. Article
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  14. Review
  15. Article
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  17. Article
  18. Expression ofJournal of clinical medicine · 2019
    Article
  19. Review
  20. Article

15 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

7 authors at 1 institution in 1 country.

Nica M BorradaileCenter for Cardiovascular Research, Division of Cardiology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Kimberly K Buhman
Laura L Listenberger
Carolyn J Magee
Emiko T A Morimoto
Daniel S Ory
Jean E Schaffer
Washington University in St. Louis · US

Funding

CELLULAR MECHANISMS THAT PROMOTE OR PREVENT LIPOTOXICITYR01DK064989 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 2003 to 2021
$5.8M
Cellular mechanisms that promotes or prevent lipotoxicityR56DK064989 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E · 2006 to 2007
$303k
NIDDK NIH HHS DK064989NIDDK NIH HHS R01 DK064989NIDDK NIH HHS R56 DK064989
6 · The paper itself

Abstract

The deleterious consequences of fatty acid (FA) and neutral lipid accumulation in nonadipose tissues, such as the heart, contribute to the pathogenesis of type 2 diabetes. To elucidate mechanisms of FA-induced cell death, or lipotoxicity, we generated Chinese hamster ovary (CHO) cell mutants resistant to palmitate-induced death and isolated a clone with disruption of eukaryotic elongation factor (eEF) 1A-1. eEF1A-1 involvement in lipotoxicity was confirmed in H9c2 cardiomyoblasts, in which small interfering RNA-mediated knockdown also conferred palmitate resistance. In wild-type CHO and H9c2 cells, palmitate increased reactive oxygen species and induced endoplasmic reticulum (ER) stress, changes accompanied by increased eEF1A-1 expression. Disruption of eEF1A-1 expression rendered these cells resistant to hydrogen peroxide- and ER stress-induced death, indicating that eEF1A-1 plays a critical role in the cell death response to these stressors downstream of lipid overload. Disruption of eEF1A-1 also resulted in actin cytoskeleton defects under basal conditions and in response to palmitate, suggesting that eEF1A-1 mediates lipotoxic cell death, secondary to oxidative and ER stress, by regulating cytoskeletal changes critical for this process. Furthermore, our observations of oxidative stress, ER stress, and induction of eEF1A-1 expression in a mouse model of lipotoxic cardiomyopathy implicate this cellular response in the pathophysiology of metabolic disease.

Indexed as

AnimalsBiomarkersCardiomyopathiesCell DeathCell LineCricetinaeCricetulusDisease Models, AnimalEndoplasmic ReticulumMiceModels, BiologicalMutagenesis, InsertionalMyocytes, CardiacOxidative StressPalmitatesPeptide Elongation Factor 1BiomarkersPalmitatesPeptide Elongation Factor 1Reactive Oxygen Species

Identifiers

PMID16319173
PMCPMC1356587
OpenAlexW2110098472

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.