Evidence map›Paper›PMID 27856258›Full record

ArticleBiochemical and biophysical research communications2017

Aspirin increases mitochondrial fatty acid oxidation.

Radha Uppala, Brianne Dudiak, Megan E Beck, Sivakama S Bharathi, Yuxun Zhang, Donna B Stolz, Eric S Goetzman

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

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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 2 institutions in 1 country.

Radha UppalaDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, United States.
Brianne DudiakDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, United States.
Megan E BeckDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, United States.
Sivakama S BharathiDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, United States.
Yuxun ZhangDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, United States.
Donna B StolzCenter for Biologic Imaging, Department of Cell Biology, University of Pittsburgh, Pittsburgh, PA 15260, United States.
Eric S GoetzmanDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, United States. Electronic address: Eric.goetzman@chp.edu.
Children's Hospital of Pittsburgh · USUniversity of Pittsburgh · US

Funding

Regulation of Peroxisomal Metabolism by Lysine AcylationR01DK090242 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOETZMAN, ERIC S · 2011 to 2024
$5.4M
NIDDK NIH HHS R01 DK090242
6 · The paper itself

Abstract

The metabolic effects of salicylates are poorly understood. This study investigated the effects of aspirin on fatty acid oxidation. Aspirin increased mitochondrial long-chain fatty acid oxidation, but inhibited peroxisomal fatty acid oxidation, in two different cell lines. Aspirin increased mitochondrial protein acetylation and was found to be a stronger acetylating agent in vitro than acetyl-CoA. However, aspirin-induced acetylation did not alter the activity of fatty acid oxidation proteins, and knocking out the mitochondrial deacetylase SIRT3 did not affect the induction of long-chain fatty acid oxidation by aspirin. Aspirin did not change oxidation of medium-chain fatty acids, which can freely traverse the mitochondrial membrane. Together, these data indicate that aspirin does not directly alter mitochondrial matrix fatty acid oxidation enzymes, but most likely exerts its effects at the level of long-chain fatty acid transport into mitochondria. The drive on mitochondrial fatty acid oxidation may be a compensatory response to altered mitochondrial morphology and inhibited electron transport chain function, both of which were observed after 24 h incubation of cells with aspirin. These studies provide insight into the pathophysiology of Reye Syndrome, which is known to be triggered by aspirin ingestion in patients with fatty acid oxidation disorders.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalAspirinCell RespirationDose-Response Relationship, DrugFatty AcidsHEK293 CellsHumansMetabolic Clearance RateMitochondriaMitochondrial ProteinsOxidation-ReductionAnti-Inflammatory Agents, Non-SteroidalAspirinFatty AcidsMitochondrial ProteinsAspirinFatty acid oxidationLysine acetylationMitochondriaPeroxisomesSIRT3

Identifiers

PMID27856258
PMCPMC5195905
OpenAlexW2557223721

What OpenQuestion holds

Textmetadata
LicenceTDM
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.