Evidence map›Paper›PMID 26886225›Full record

ReviewHeart failure reviews2016

Mitochondrial involvement in myocyte death and heart failure.

Michael J Goldenthal

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  14. NETosis as a Pathogenic Factor for Heart Failure.Oxidative medicine and cellular longevity · 2021
    Review
  15. Article
  16. Metabolic Imaging in Cardio-oncology.Journal of cardiovascular translational research · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

1 author at 1 institution in 1 country.

Michael J GoldenthalSt. Christopher's Hospital for Children, Drexel University College of Medicine, Philadelphia, PA, 19134, USA. migojo2@yahoo.com.
Drexel University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the heart is an energy-demanding organ, impaired cardiac energy metabolism and mitochondrial function have been inexorably linked to cardiac dysfunction. There is a growing recognition that mitochondrial dysfunction contributes to impaired myocardial energetics and increased oxidative stress in cardiomyopathies, cardiac ischemic damage and heart failure (HF), and mitochondrial permeability transition pore opening has been reported a critical trigger of myocyte death and myocardial remodeling. It is well established that mitochondria play pivotal roles in intracellular signaling in both cell death as well as in cardioprotective pathways. Moreover, recent studies have shown that defects in mitochondrial dynamics affecting biogenesis and turnover are linked to cardiac senescence and HF. Accordingly, there has been an increasing interest in targeting mitochondria for HF therapy. This article reviews the background and recent evidence of mitochondrial involvement in several types of cell death (apoptosis, necrosis and autophagy) occurring in HF. In addition, potential strategies for targeting mitochondria are examined, and their utility in HF therapy considered.

Indexed as

Cell DeathEnergy MetabolismHeart FailureHumansMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocytes, CardiacOxidative StressRandomized Controlled Trials as TopicReactive Oxygen SpeciesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen SpeciesApoptosisAutophagyMitochondriaNecrosisPermeabilityPore

Identifiers

PMID26886225
OpenAlexW2278414986

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.