Evidence map›Paper›PMID 25640959›Full record

ReviewMitochondrion2015

Mitochondrial Diseases Part II: Mouse models of OXPHOS deficiencies caused by defects in regulatory factors and other components required for mitochondrial function.

Luisa Iommarini, Susana Peralta, Alessandra Torraco, Francisca Diaz

Abstract 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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.

  1. Article
  2. Mitochondrial Transplantation as a Therapeutic Strategy for Inherited Mitochondrial Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. The Peroxisome-Mitochondria Connection: How and Why?International journal of molecular sciences · 2017
    Review
  12. Review: Central nervous system involvement in mitochondrial disease.Neuropathology and applied neurobiology · 2017
    Review
  13. Article
  14. Review
  15. Review
  16. 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

4 authors.

Luisa IommariniDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Via Irnerio 42, 40128 Bologna, Italy. Electronic address: luisa.iommarini2@unibo.it.
Susana PeraltaDepartment of Neurology, University of Miami, Miller School of Medicine, Miami, FL 33136, USA. Electronic address: SPeralta@med.miami.edu.
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.
Francisca DiazDepartment of Neurology, University of Miami, Miller School of Medicine, Miami, FL 33136, USA. Electronic address: fdiaz1@med.miami.edu.

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 defined as defects that affect the oxidative phosphorylation system (OXPHOS). They are characterized by a heterogeneous array of clinical presentations due in part to a wide variety of factors required for proper function of the components of the OXPHOS system. There is no cure for these disorders owing to our poor knowledge of the pathogenic mechanisms of disease. To understand the mechanisms of human disease numerous mouse models have been developed in recent years. Here we summarize the features of several mouse models of mitochondrial diseases directly related to those factors affecting mtDNA maintenance, replication, transcription, translation as well as other proteins that are involved in mitochondrial dynamics and quality control which affect mitochondrial OXPHOS function without being intrinsic components of the system. We discuss how these models have contributed to our understanding of mitochondrial diseases and their pathogenic mechanisms.

Indexed as

Oxidative PhosphorylationAnimalsDisease Models, AnimalHumansMiceMitochondrial DiseasesMitochondrial diseasesMitochondrial DNAMitochondrial dynamicsMitochondrial transcriptionMouse modelsQuality control

Identifiers

PMID25640959
PMCPMC4447541

What OpenQuestion holds

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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.