Evidence map›Paper›PMID 22103917›Full record

ReviewCongestive heart failure (Greenwich, Conn.)

Proteomic remodeling of mitochondria in heart failure.

John M Hollander, Walter A Baseler, Erinne R Dabkowski

Open access · bronzeAbstract readReview
In one paragraph

Review in Congestive heart failure (Greenwich, Conn.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Heart Metabolism in Sepsis-Induced Cardiomyopathy-Unusual Metabolic Dysfunction of the Heart.International journal of environmental research and public health · 2021
    Review
  2. Article
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  4. Article
  5. Calcineurin signaling in the heart: The importance of time and place.Journal of molecular and cellular cardiology · 2017
    Review
  6. Role of microRNA in metabolic shift during heart failure.American journal of physiology. Heart and circulatory physiology · 2017
    Review
  7. Review
  8. Review
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  10. Article
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  15. Article
  16. Differential regulation of EHD3 in human and mammalian heart failure.Journal of molecular and cellular cardiology · 2012
    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

3 authors at 1 institution in 1 country.

John M HollanderDivision of Exercise Physiology and Center for Cardiovascular and Respiratory Sciences, West Virginia University School of Medicine, Morgantown, USA. jhollander@hsc.wvu.edu
Walter A Baseler
Erinne R Dabkowski
West Virginia University · US

Funding

Mechanisms of Diabetic Cardiomyopathy: Mitochondria Subpopulations Brought to FocDP2DK083095 · NIDDK · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2008 to 2010
$2.3M
NIDDK NIH HHS DP2 DK083095NIDDK NIH HHS DP2DK083095
6 · The paper itself

Abstract

Heart failure (HF) is a common disease that has been attributed, in part, to deprivation of cardiac energy. As a result, the interplay between metabolism and adenosine triphosphate production is fundamental in determining the mechanisms driving the disease progression. Due to its central role in energy production, metabolism, calcium homeostasis, and oxidative stress, the mitochondrion has been suggested to play a pivotal role in the progression of the heart to failure. Nevertheless, the mitochondrion's specific role(s) and the proteins contributing to the development and progression of HF are not entirely clear. Thus, changes in mitochondrial proteomic make-up during HF have garnered great interest. With the continued development of advanced tools for assessing proteomic make-up, characterization of mitochondrial proteomic changes during disease states such as HF are being realized. These studies have begun to identify potential biomarkers of disease progression as well as protein targets that may provide an avenue for therapeutic intervention. The goal of this review is to highlight some of the changes in mitochondrial proteomic make-up that are associated with the development of HF in an effort to identify target axes and candidate proteins contributing to disease development. Results from a number of different HF models will be evaluated to gain insight into some of the similarities and differences in mitochondrial proteomic alterations associated with morphological and functional changes that result from the disease. Congest Heart Fail.

Indexed as

Energy MetabolismAdenosine TriphosphateAnimalsApoptosisHeart FailureHumansMitochondria, HeartOxidative StressProteomeReactive Oxygen SpeciesAdenosine TriphosphateProteomeReactive Oxygen Species

Identifiers

PMID22103917
PMCPMC3229269
OpenAlexW1870516439

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.