Evidence map›Paper›PMID 23328733›Full record

ArticleFree radical biology & medicine2013

4-Hydroxy-2(E)-nonenal (HNE) catabolism and formation of HNE adducts are modulated by β oxidation of fatty acids in the isolated rat heart.

Qingling Li, Sushabhan Sadhukhan, Jessica M Berthiaume, Rafael A Ibarra, Hui Tang, Shuang Deng, Eric Hamilton, Laura E Nagy, Gregory P Tochtrop, Guo-Fang Zhang

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
  2. Review
  3. ACAD10 and ACAD11 enable mammalian 4-hydroxy acid lipid catabolism.Nature structural & molecular biology · 2025
    Article
  4. The unique reactivity of EKODE lipid peroxidation products allows in vivo detection of inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. 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

10 authors at 2 institutions in 1 country.

Qingling LiDepartment of Nutrition, Case Western Reserve University, Cleveland, OH 44106, USA.
Sushabhan Sadhukhan
Jessica M Berthiaume
Rafael A Ibarra
Hui Tang
Shuang Deng
Eric Hamilton
Laura E Nagy
Gregory P Tochtrop
Guo-Fang Zhang
Case Western Reserve University · USCleveland Clinic · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Role of Adipose in Ethanol-Induced Tissue InjuryR37AA011876 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2009 to 2018
$4.0M
Dynamic Metabolomics via Isotopomer Analysis(RMI)R33DK070291 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUNENGRABER, HENRI · 2004 to 2006
$3.3M
Metabolomic and Isotopomer Analysis of Xenobiotic StressR01ES013925 · NIEHS · CASE WESTERN RESERVE UNIVERSITY · PI BRUNENGRABER, HENRI · 2005 to 2009
$2.7M
Mouse Metabolic Phenotyping CenterU24DK076174 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUNENGRABER, HENRI · 2011 to 2015
$2.7M
Triterpenoid Modulators of Inflammatory Driven CarcinogenesisR01CA157735 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI TOCHTROP, GREGORY P · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA157735NCI NIH HHS R01CA157735NCRR NIH HHS UL1 RR024989NCRR NIH HHS UL1RR024989NIAAA NIH HHS 5R37AA011876NIAAA NIH HHS R37 AA011876NIDDK NIH HHS R33 DK070291NIDDK NIH HHS R33DK070291NIDDK NIH HHS U24 DK076174NIEHS NIH HHS R01 ES013925NIEHS NIH HHS R01ES013925
6 · The paper itself

Abstract

We previously reported that a novel metabolic pathway functionally catabolizes 4-hydroxy-2(E)-nonenal (HNE) via two parallel pathways, which rely heavily on β-oxidation pathways. The hypothesis driving this report is that perturbations of β oxidation will alter the catabolic disposal of HNE, favoring an increase in the concentrations of HNE and HNE-modified proteins that may further exacerbate pathology. This study employed Langendorff perfused hearts to investigate the impact of cardiac injury modeled by ischemia/reperfusion and, in a separate set of perfusions, the effects of elevated lipid (typically observed in obesity and type II diabetes) by perfusing with increased fatty acid concentrations (1mM octanoate). During ischemia, HNE concentrations doubled and the glutathione-HNE adduct and 4-hydroxynonanoyl-CoA were increased by 7- and 10-fold, respectively. Under conditions of increased fatty acid, oxidation to 4-hydroxynonenoic acid was sustained; however, further catabolism through β oxidation was nearly abolished. The inhibition of HNE catabolism was not compensated for by other disposal pathways of HNE, rather an increase in HNE-modified proteins was observed. Taken together, this study presents a mechanistic rationale for the accumulation of HNE and HNE-modified proteins in pathological conditions that involve alterations to β oxidation, such as myocardial ischemia, obesity, and high-fat diet-induced diseases.

Indexed as

Lipid MetabolismAnimalsFatty AcidsFatty Acids, UnsaturatedGlutathioneHydroxy AcidsMaleMyocardiumOrgan Culture TechniquesRatsReperfusion Injury4-hydroxynonenoic acidFatty AcidsFatty Acids, UnsaturatedGlutathioneHydroxy Acids

Identifiers

PMID23328733
PMCPMC3723455
OpenAlexW1989638490

What OpenQuestion holds

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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.