Evidence map›Paper›PMID 24136824›Full record

ArticleJournal of lipid research2014

Docosahexaenoic acid impairs the maturation of very low density lipoproteins in rat hepatic cells.

Vatsala Maitin, Ursula Andreo, Liang Guo, Edward A Fisher

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. DietaryNutrients · 2025
    Article
  2. Review
  3. Can modulators of apolipoproteinB biogenesis serve as an alternate target for cholesterol-lowering drugs?Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018
    Review
  4. Article
  5. Regression of Atherosclerosis: The Journey From the Liver to the Plaque and Back.Arteriosclerosis, thrombosis, and vascular biology · 2016
    Review
  6. Hyperlipoproteinemia type 3: the forgotten phenotype.Current atherosclerosis reports · 2014
    Review
  7. Article
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.

Vatsala MaitinDepartments of Medicine (Leon H. Charney Division of Cardiology) and Cell Biology and the Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY 10016; and.
Ursula Andreo
Liang Guo
Edward A Fisher
New York University · USTexas State University · US

Funding

MOLECULAR REGULATION OF APOPROTEIN B DEGRADATIONR01HL058541 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 1997 to 2014
$4.4M
Molecular Regulation of Apoprotein B DegradationR01HL127930 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2016 to 2019
$1.7M
NHLBI NIH HHS R01 HL058541NHLBI NIH HHS R01 HL127930
6 · The paper itself

Abstract

One mechanism of the lipid-lowering effects of the fish oil n-3 fatty acids [e.g., docosahexaenoic acid (DHA)] in cell and animal models is induced hepatic apolipoprotein B100 (apoB) presecretory degradation. This degradation occurs post-endoplasmic reticulum, but whether DHA induces it before or after intracellular VLDL formation remains unanswered. We found in McA-RH7777 rat hepatic cells that DHA and oleic acid (OA) treatments allowed formation of pre-VLDL particles and their transport to the Golgi, but, in contrast to OA, with DHA pre-VLDL particles failed to quantitatively assemble into fully lipidated (mature) VLDL. This failure required lipid peroxidation and was accompanied by the formation of apoB aggregates (known to be degraded by autophagy). Preventing the exit of proteins from the Golgi blocked the aggregation of apoB but did not restore VLDL maturation, indicating that failure to fully lipidate apoB preceded its aggregation. ApoB autophagic degradation did not appear to require an intermediate step of cytosolic aggresome formation. Taken with other examples in the literature, the results of this study suggest that pre-VLDL particles that are competent to escape endoplasmic reticulum quality control mechanisms but fail to mature in the Golgi remain subject to quality control surveillance late in the secretory pathway.

Indexed as

AnimalsApolipoproteins BCell Line, TumorDocosahexaenoic AcidsGolgi ApparatusHepatocytesLipid PeroxidationLipoproteins, VLDLLysosomesMicrosomes, LiverMicrotubulesRatsApolipoproteins BDocosahexaenoic AcidsLipoproteins, VLDLapoBautophagyendoplasmic reticulumGolgilipid peroxidation

Identifiers

PMID24136824
PMCPMC3927475
OpenAlexW2115374154

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.