Evidence map›Paper›PMID 22066679›Full record

ReviewClinical and experimental pharmacology & physiology2012

Mitochondria as a source and target of lipid peroxidation products in healthy and diseased heart.

Ethan J Anderson, Lalage A Katunga, Monte S Willis

Abstract readReview
In one paragraph

Review in Clinical and experimental pharmacology & physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

66 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Annals of medicine · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Lipotoxicity: a driver of heart failure with preserved ejection fraction?Clinical science (London, England : 1979) · 2021
    Review
  20. A chemical field guide to histone nonenzymatic modifications.Current opinion in chemical biology · 2021
    Review

6 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

3 authors at 3 institutions in 2 countries.

Ethan J AndersonDepartment of Medicine, Pathology & Laboratory Medicine, 111 Mason Farm Road, 2340BMBRB,Chapel Hill, NC 27599–7525, USA.
Lalage A Katunga
Monte S Willis
Cardiovascular Research Center · BREast Carolina University · USUniversity of North Carolina at Chapel Hill · US

Funding

Myocyte specific regulation of metabolism and the response to biomechanical forceR01HL104129 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILLIS, MONTE S · 2010 to 2018
$3.3M
Linking redox chemistry and mitochondria in atrium to post-operative arrhythmiaR21HL098780 · NHLBI · EAST CAROLINA UNIVERSITY · PI ANDERSON, ETHAN JOHN · 2010 to 2011
$395k
NHLBI NIH HHS R01 HL104129NHLBI NIH HHS R01HL104129NHLBI NIH HHS R21 HL098780NHLBI NIH HHS R21HL098780
6 · The paper itself

Abstract

The heart is a highly oxidative organ in which cardiomyocyte turnover is virtually absent, making it particularly vulnerable to accumulation of lipid peroxidation products (LPP) formed as a result of oxidative damage. Reactive oxygen and nitrogen species are the most common electrophiles formed during lipid peroxidation and lead to the formation of both stable and unstable LPP. Of the LPP formed, highly reactive aldehydes are a well-recognized causative factor in ageing and age-associated diseases, including cardiovascular disease and diabetes. Recent studies have identified that the mitochondria are both a primary source and target of LPP, with specific emphasis on aldehydes in cardiomyocytes and how these affect the electron transport system and Ca(2+) balance. Numerous studies have found that there are functional consequences in the heart following exposure to specific aldehydes (acrolein, trans-2-hexanal, 4-hydroxynonenal and acetaldehyde). Because these LPP are known to form in heart failure, cardiac ischaemia-reperfusion injury and diabetes, they may have an underappreciated role in the pathophysiology of these disease processes. Lipid peroxidation products are involved in the transcriptional regulation of endogenous anti-oxidant systems. Recent evidence demonstrates that transient increases in LPP may be beneficial in cardioprotection by contributing to mitohormesis (i.e. induction of anti-oxidant systems) in cardiomyocytes. Thus, exploitation of the cardioprotective actions of the LPP may represent a novel therapeutic strategy for future treatment of heart disease.

Indexed as

Lipid PeroxidationAnimalsAntioxidantsHeartHeart DiseasesHumansMitochondriaOxidative StressAntioxidants

Identifiers

PMID22066679
PMCPMC3827773
OpenAlexW2138632104

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.