Evidence map›Paper›PMID 25918579›Full record

ReviewOxidative medicine and cellular longevity2015

The mitochondrial translocator protein and arrhythmogenesis in ischemic heart disease.

Lukas J Motloch, Jun Hu, Fadi G Akar

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2015. 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
1.7field-weighted citation impact, top 16% 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, 32 citations in OpenAlex.

  1. Article
  2. Review
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  4. MIAT, a potent CVD-promoting lncRNA.Cellular and molecular life sciences : CMLS · 2021
    Article
  5. [Annals of nuclear medicine · 2021
    Article
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  8. Article
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  13. Article
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  15. Article
  16. Functional Role of Mitochondria in Arrhythmogenesis.Advances in experimental medicine and biology · 2017
    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

3 authors at 1 institution in 1 country.

Lukas J MotlochCardiovascular Institute, Icahn School of Medicine at Mount Sinai, Hess Center for Science & Medicine, One Gustave L. Levy Place, P.O. Box 1030, New York, NY 1002, USA.ORCID 0000-0003-2832-6582
Jun HuCardiovascular Institute, Icahn School of Medicine at Mount Sinai, Hess Center for Science & Medicine, One Gustave L. Levy Place, P.O. Box 1030, New York, NY 1002, USA.ORCID 0000-0002-7013-0703
Fadi G AkarCardiovascular Institute, Icahn School of Medicine at Mount Sinai, Hess Center for Science & Medicine, One Gustave L. Levy Place, P.O. Box 1030, New York, NY 1002, USA.
Icahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is a hallmark of multiple cardiovascular disorders, including ischemic heart disease. Although mitochondria are well recognized for their role in energy production and cell death, mechanisms by which they control excitation-contraction coupling, excitability, and arrhythmias are less clear. The translocator protein (TSPO) is an outer mitochondrial membrane protein that is expressed in multiple organ systems. The abundant expression of TSPO in macrophages has been leveraged to image the immune response of the heart to inflammatory processes. More recently, the recognition of TSPO as a regulator of energy-dissipating mitochondrial pathways has extended its utility from a diagnostic marker of inflammation to a therapeutic target influencing diverse pathophysiological processes. Here, we provide an overview of the emerging role of TSPO in ischemic heart disease. We highlight the importance of TSPO in the regenerative process of reactive oxygen species (ROS) induced ROS release through its effects on the inner membrane anion channel (IMAC) and the permeability transition pore (PTP). We discuss evidence implicating TSPO in arrhythmogenesis in the settings of acute ischemia-reperfusion injury and myocardial infarction.

Indexed as

HumansIon ChannelsMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial IschemiaOxidative StressReactive Oxygen SpeciesIon ChannelsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen Species

Identifiers

PMID25918579
PMCPMC4397036
OpenAlexW2029310150

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.