Evidence map›Paper›PMID 24548633›Full record

ArticleLife sciences2014

Mitochondrial proteome remodeling in ischemic heart failure.

Tingting Liu, Le Chen, Eunjung Kim, Diana Tran, Brett S Phinney, Anne A Knowlton

Abstract read
In one paragraph

Article in Life sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025
    Review
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  8. Article
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  14. Review
  15. Review
  16. Article
  17. Real time mitochondrial dimension measurements.Journal of biological methods · 2019
    Article
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Tingting LiuMolecular & Cellular Cardiology, Cardiovascular Division, University of California - Davis, Davis, CA, USA.
Le ChenMolecular & Cellular Cardiology, Cardiovascular Division, University of California - Davis, Davis, CA, USA.
Eunjung KimClinical Research, St. Mary's Hospital of Daejeon Catholic University, Daejeon, Republic of Korea.
Diana TranProteomics Core Facility, University of California - Davis, Davis, CA, USA.
Brett S PhinneyProteomics Core Facility, University of California - Davis, Davis, CA, USA.
Anne A KnowltonMolecular & Cellular Cardiology, Cardiovascular Division, University of California - Davis, Davis, CA, USA; Pharmacology Department, University of California - Davis, Davis, CA, USA; VA Medical Center Sacramento, CA, USA. Electronic address: aaknowlton@ucdavis.edu.
University of California, Davis · USThe Catholic University of Korea Daejeon St. Mary's Hospital · KR

Funding

Human Cardiomyopathy and HSP60R01HL077281 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI KNOWLTON, ANNE A · 2004 to 2012
$3.1M
HSPs, Inflammatory Response and Cardiovascular DiseaseR01HL079071 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KNOWLTON, ANNE A · 2006 to 2014
$2.7M
In Vivo Ultrasound Imaging System (VEVO 2100, VisualSonics)S10OD010389 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2013 to 2013
$397k
NHLBI NIH HHS HL077281NHLBI NIH HHS HL079071NHLBI NIH HHS R01 HL077281NHLBI NIH HHS R01 HL079071NIH HHS S10 OD010389
6 · The paper itself

Abstract

aimsMitochondrial dysfunction is an important part of the decline in cardiac function in heart failure. We hypothesized for hypothesized that there would be specific abnormalities in mitochondrial function and proteome with the progression of ischemic heart failure (HF). MAIN

methodsWe used a high left anterior descending artery (LAD) ligation in 3-4month old male rats to generate HF. Rats were studied 9weeks post-ligation. KEY

findingsElectron microscopy of left ventricle samples showed mitochondrial changes including decreased size, increased number, abnormal distribution, and cristae loss. Mitochondria in ischemic HF exhibited decreased total ATP, impaired mitochondrial respiration, as well as reduced complex I activity. Analysis of LV mitochondrial proteins by mass spectrometry was performed, and 31 differentially expressed proteins (p<0.05) of more than 500 total proteins were identified. Of these proteins, 15 were up-regulated and 16 were down-regulated in the failing heart. A set of complex I proteins was significantly decreased, consistent with the impairment of complex I activity. There were distinct changes in mitochondrial function and proteome in ischemic HF. Although there were similarities, the distinction between the reported proteomic changed with TAC pressure overload induced HF and ischemic HF in the current study suggested different pathological mechanisms. SIGNIFICANCE: Specific changes in mitochondrial protein expression, which correlate with changes in mitochondrial function, have been identified in ischemic HF for the first time.

Indexed as

Adenosine TriphosphateAnimalsDown-RegulationElectron Transport Complex IElectron Transport Complex IIElectron Transport Complex IVHeart FailureMaleMitochondria, HeartMitochondrial ProteinsMyocardial IschemiaOxygen ConsumptionProteomeRatsSignal TransductionUp-RegulationAdenosine TriphosphateElectron Transport Complex IElectron Transport Complex IIElectron Transport Complex IVMitochondrial ProteinsProteomeComplex IComplex IIComplex IVHeartHeart failureIschemic heart failureMitochondriaNADH dehydrogenaseNDUFA5NDUFV1Proteome remodeling

Identifiers

PMID24548633
PMCPMC4075482
OpenAlexW2048447205

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.