Evidence map›Paper›PMID 18185992›Full record

ReviewHeart failure reviews2008

Mitochondrial centrality in heart failure.

José Marín-García, Michael J Goldenthal

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

62 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  20. Mitochondrial structure and function are not different between nonfailing donor and end-stage failing human hearts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article

2 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

2 authors.

José Marín-GarcíaThe Molecular Cardiology and Neuromuscular Institute, 75 Raritan Ave., Highland Park, NJ 08904, USA. tmci@att.net
Michael J Goldenthal

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A number of observations have shown that mitochondria are at the center of the pathophysiology of the failing heart and mitochondrial-based oxidative stress (OS), myocardial apoptosis, and cardiac bioenergetic dysfunction are implicated in the progression of heart failure (HF), as shown by both clinical studies and animal models. In this manuscript, we review the body of evidence that multiple defects in mitochondria are central and primary to HF progression. In addition, novel approaches to therapeutic targeting of mitochondrial bioenergetic, biogenic, and signaling abnormalities that can impact HF are discussed.

Indexed as

Adenosine TriphosphateAnimalsApoptosisEnergy MetabolismHeart FailureHumansMitochondria, HeartOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateReactive Oxygen Species

Identifiers

PMID18185992

What OpenQuestion holds

Textmetadata
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.