Evidence map›Paper›PMID 28190190›Full record

ReviewCardiovascular drugs and therapy2017

Mitochondrial-Shaping Proteins in Cardiac Health and Disease - the Long and the Short of It!

Sang-Bing Ong, Siavash Beikoghli Kalkhoran, Sauri Hernández-Reséndiz, Parisa Samangouei, Sang-Ging Ong, Derek John Hausenloy

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cardiovascular drugs and therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
5.7field-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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

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  18. Neurohormonal connections with mitochondria in cardiomyopathy and other diseases.American journal of physiology. Cell physiology · 2022
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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 3 institutions in 3 countries.

Sang-Bing OngCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, 8 College Road, Singapore, 169857, Singapore.
Siavash Beikoghli KalkhoranThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK.
Sauri Hernández-ReséndizCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, 8 College Road, Singapore, 169857, Singapore.
Parisa SamangoueiThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, London, UK.
Sang-Ging OngStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA.
Derek John HausenloyCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, 8 College Road, Singapore, 169857, Singapore. derek.hausenloy@duke-nus.edu.sg.
National Heart Centre Singapore · SGNational University of Singapore · SGUniversity College London · GB

Funding

Cardiac Mitohormesis Protects Against Diabetic Cardiomyopathy Through MitophagyK99HL130416 · NHLBI · STANFORD UNIVERSITY · PI ONG, SANG GING · 2016 to 2017
$258k
British Heart Foundation FS/10/039/28270British Heart Foundation FS/10/39/28270British Heart Foundation FS/13/41/30368Medical Research Council MR/J003530/1NHLBI NIH HHS K99 HL130416
6 · The paper itself

Abstract

Mitochondrial health is critically dependent on the ability of mitochondria to undergo changes in mitochondrial morphology, a process which is regulated by mitochondrial shaping proteins. Mitochondria undergo fission to generate fragmented discrete organelles, a process which is mediated by the mitochondrial fission proteins (Drp1, hFIS1, Mff and MiD49/51), and is required for cell division, and to remove damaged mitochondria by mitophagy. Mitochondria undergo fusion to form elongated interconnected networks, a process which is orchestrated by the mitochondrial fusion proteins (Mfn1, Mfn2 and OPA1), and which enables the replenishment of damaged mitochondrial DNA. In the adult heart, mitochondria are relatively static, are constrained in their movement, and are characteristically arranged into 3 distinct subpopulations based on their locality and function (subsarcolemmal, myofibrillar, and perinuclear). Although the mitochondria are arranged differently, emerging data supports a role for the mitochondrial shaping proteins in cardiac health and disease. Interestingly, in the adult heart, it appears that the pleiotropic effects of the mitochondrial fusion proteins, Mfn2 (endoplasmic reticulum-tethering, mitophagy) and OPA1 (cristae remodeling, regulation of apoptosis, and energy production) may play more important roles than their pro-fusion effects. In this review article, we provide an overview of the mitochondrial fusion and fission proteins in the adult heart, and highlight their roles as novel therapeutic targets for treating cardiac disease.

Indexed as

Mitochondrial DynamicsAnimalsApoptosisEnergy MetabolismHeart DiseasesHumansMitochondria, HeartMitochondrial ProteinsMitophagyMyocardiumNecrosisSignal TransductionMitochondrial ProteinsDrp1Ischemia/reperfusion injuryMfn1Mfn2Mitochondrial fissionMitochondrial fusionMitochondrial morphologyOPA1

Identifiers

PMID28190190
PMCPMC5346600
OpenAlexW2586331924

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.