Evidence map›Paper›PMID 30338314›Full record

ArticleConditioning medicine2018

MiD49 and MiD51: New mediators of mitochondrial fission and novel targets for cardioprotection.

Parisa Samangouei, Gustavo E Crespo-Avilan, Hector Cabrera-Fuentes, Sauri Hernández-Reséndiz, Nur Izzah Ismail, Khairunnisa Binte Katwadi, William A Boisvert, Derek J Hausenloy

Open access · greenAbstract read
In one paragraph

Article in Conditioning medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  4. Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025
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  11. Review
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  13. Review
  14. Review
  15. Review
  16. Article
  17. Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Article
  20. 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

8 authors at 3 institutions in 3 countries.

Parisa SamangoueiHatter Cardiovascular Institute, University College London, UK.
Gustavo E Crespo-AvilanCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore.
Hector Cabrera-FuentesCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore.
Sauri Hernández-ReséndizCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore.
Nur Izzah IsmailCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore.
Khairunnisa Binte KatwadiCardiovascular and Metabolic Disorders Program, Duke-National University of Singapore.
William A BoisvertDepartment of Biomedical Engineering, Faculty of Engineering, University of Malaya , Kuala Lumpur , Malaysia.
Derek J HausenloyHatter Cardiovascular Institute, University College London, UK.
National Heart Centre Singapore · SGNational University of Singapore · SGUniversity of Malaya · MY

Funding

Rho kinase in immune-mediated atherosclerosisR01HL081863 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI BOISVERT, WILLIAM A · 2007 to 2010
$1.6M
ACTIN CAPPING PROTEINS IN PLATELETS AND MUSCLEK08HL001341 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CASELLA, JAMES F · 1985 to 1988
–
British Heart Foundation FS/10/39/28270British Heart Foundation FS/13/41/30368Medical Research Council MR/J003530/1NHLBI NIH HHS R01 HL081863
6 · The paper itself

Abstract

Acute myocardial infarction (AMI) and the heart failure (HF) that often follows are among the leading causes of death and disability worldwide. As such novel therapies are needed to reduce myocardial infarct (MI) size, and preserve left ventricular (LV) systolic function in order to reduce the propensity for HF following AMI. Mitochondria are dynamic organelles that can undergo morphological changes by two opposing processes, mitochondrial fusion and fission. Changes in mitochondrial morphology and turnover are a vital part of maintaining mitochondrial health, DNA stability, energy production, calcium homeostasis, cellular division, and differentiation, and disturbances in the balance of fusion and fission can predispose to mitochondrial dysfunction and cell death. Changes in mitochondrial morphology are governed by mitochondrial fusion proteins (Mfn1, Mfn2 and OPA1) and mitochondrial fission proteins (Drp1, hFis1, and Mff). Recent experimental data suggest that mitochondria undergo fission during acute ischemia/reperfusion injury (IRI), generating fragmented dysfunctional mitochondrial and predisposing to cell death. We and others have shown that genetic and pharmacological inhibition of the mitochondrial fission protein Drp1 can protect cardiomyocytes from acute IRI and reduce MI size. Novel components of the mitochondrial fission machinery, mitochondrial dynamics proteins of 49 kDa (MiD49) and mitochondrial dynamics proteins of 51 kDa (MiD51), have been recently described, which have been shown to mediating mitochondrial fission by targeting Drp1 to the mitochondrial surface. In this review article, we provide an overview of MiD49 and MiD51, and highlight their potential as novel therapeutic targets for treating cardiovascular diseases such as AMI, anthracycline cardiomyopathy, and pulmonary arterial hypertension.

Indexed as

cardioprotectionDrp1MiD49MiD51Mitochondrial dynamicsmitochondrial fissionmitochondrial fusion

Identifiers

PMID30338314
PMCPMC6191188
OpenAlexW2922328919

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.