Evidence map›Paper›PMID 25660179›Full record

ReviewMitochondrion2015

Mitochondrial Diseases Part I: mouse models of OXPHOS deficiencies caused by defects in respiratory complex subunits or assembly factors.

Alessandra Torraco, Susana Peralta, Luisa Iommarini, Francisca Diaz

Open access · greenAbstract readReview
In one paragraph

Review in Mitochondrion, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. The Blood-Brain Barrier Is Unaffected in theInternational journal of molecular sciences · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. The Peroxisome-Mitochondria Connection: How and Why?International journal of molecular sciences · 2017
    Review
  18. Review: Central nervous system involvement in mitochondrial disease.Neuropathology and applied neurobiology · 2017
    Review
  19. Review
  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

4 authors at 3 institutions in 2 countries.

Alessandra TorracoUnit for Neuromuscular and Neurodegenerative Disorders, Laboratory of Molecular Medicine, Bambino Gesù Children's Hospital, IRCCS, Viale di San Paolo, 15-00146 Rome, Italy. Electronic address: alessandra.torraco@opbg.net.
Susana PeraltaDepartment of Neurology, University of Miami, Miller School of Medicine, Miami, FL 33136, USA. Electronic address: SPeralta@med.miami.edu.
Luisa IommariniDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Via Irnerio 42, 40126 Bologna, Italy. Electronic address: luisa.iommarini2@unibo.it.
Francisca DiazDepartment of Neurology, University of Miami, Miller School of Medicine, Miami, FL 33136, USA. Electronic address: fdiaz1@med.miami.edu.
University of Miami · USBambino Gesù Children's Hospital · ITUniversity of Bologna · IT

Funding

Hypoxic stabilization of OXPHOS complexes in mitochondrial defectsR01GM101225 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DIAZ, FRANCISCA · 2012 to 2016
$1.3M
NIGMS NIH HHS GM101225NIGMS NIH HHS R01 GM101225
6 · The paper itself

Abstract

Mitochondrial disorders are the most common inborn errors of metabolism affecting the oxidative phosphorylation system (OXPHOS). Because of the poor knowledge of the pathogenic mechanisms, a cure for these disorders is still unavailable and all the treatments currently in use are supportive more than curative. Therefore, in the past decade a great variety of mouse models have been developed to assess the in vivo function of several mitochondrial proteins involved in human diseases. Due to the genetic and physiological similarity to humans, mice represent reliable models to study the pathogenic mechanisms of mitochondrial disorders and are precious to test new therapeutic approaches. Here we summarize the features of several mouse models of mitochondrial diseases directly related to defects in subunits of the OXPHOS complexes or in assembly factors. We discuss how these models recapitulate many human conditions and how they have contributed to the understanding of mitochondrial function in health and disease.

Indexed as

Disease Models, AnimalOxidative PhosphorylationAnimalsHumansMiceMitochondrial DiseasesMitochondrial ProteinsMitochondrial ProteinsMitochondriaMitochondrial diseasesMouse modelsOxidative phosphorylationOXPHOS

Identifiers

PMID25660179
PMCPMC4364530
OpenAlexW2059793002

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.