Evidence map›Paper›PMID 33578638›Full record

ReviewGenes2021

Mitochondrial Dynamics: Molecular Mechanisms, Related Primary Mitochondrial Disorders and Therapeutic Approaches.

Michela Di Nottia, Daniela Verrigni, Alessandra Torraco, Teresa Rizza, Enrico Bertini, Rosalba Carrozzo

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  12. Mechanism of static loading injury in human skeletal muscle cells.American journal of translational research · 2024
    Article
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  15. Mechanistic study of optic atrophy 1 in ischemia-reperfusion disease.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
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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 1 institution in 1 country.

Michela Di NottiaLaboratory of Molecular Medicine, Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.
Daniela VerrigniLaboratory of Molecular Medicine, Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.
Alessandra TorracoLaboratory of Molecular Medicine, Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.
Teresa RizzaLaboratory of Molecular Medicine, Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.
Enrico BertiniLaboratory of Molecular Medicine, Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.ORCID 0000-0001-9276-4590
Rosalba CarrozzoLaboratory of Molecular Medicine, Unit of Muscular and Neurodegenerative Disorders, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.
Bambino Gesù Children's Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria do not exist as individual entities in the cell-conversely, they constitute an interconnected community governed by the constant and opposite process of fission and fusion. The mitochondrial fission leads to the formation of smaller mitochondria, promoting the biogenesis of new organelles. On the other hand, following the fusion process, mitochondria appear as longer and interconnected tubules, which enhance the communication with other organelles. Both fission and fusion are carried out by a small number of highly conserved guanosine triphosphatase proteins and their interactors. Disruption of this equilibrium has been associated with several pathological conditions, ranging from cancer to neurodegeneration, and mutations in genes involved in mitochondrial fission and fusion have been reported to be the cause of a subset of neurogenetic disorders.

Indexed as

ATPases Associated with Diverse Cellular ActivitiesDynaminsGene Expression RegulationGTP PhosphohydrolasesHumansMembrane ProteinsMetalloendopeptidasesMitochondriaMitochondrial DiseasesMitochondrial DynamicsMitochondrial ProteinsNeoplasmsNeurodegenerative DiseasesOrganelle BiogenesisPeptide Elongation FactorsProtective AgentsATPases Associated with Diverse Cellular ActivitiesDNM1L protein, humanDynaminsGTP PhosphohydrolasesMembrane ProteinsMetalloendopeptidasesMff protein, humanMFN2 protein, humanMIEF2 protein, humanMitochondrial ProteinsOPA1 protein, humanPeptide Elongation FactorsProtective AgentsYME1L1 protein, humanmitochondrial diseasesmitochondrial dynamicstherapeutic approaches

Identifiers

PMID33578638
PMCPMC7916359
OpenAlexW3127187310

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.