Evidence map›Paper›PMID 28835707›Full record

ArticleScientific reports2017

Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities.

Valentina Di Pietro, Giacomo Lazzarino, Angela Maria Amorini, Stefano Signoretti, Lisa J Hill, Edoardo Porto, Barbara Tavazzi, Giuseppe Lazzarino, Antonio Belli

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.3field-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

59 citing papers in PubMed, 87 citations in OpenAlex.

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  12. Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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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

9 authors at 4 institutions in 3 countries.

Valentina Di PietroNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK.
Giacomo LazzarinoInstitute of Biochemistry and Clinical Biochemistry, Catholic University of Rome, Largo F. Vito 1, 00168, Rome, Italy.
Angela Maria AmoriniInstitute of Biochemistry and Clinical Biochemistry, Catholic University of Rome, Largo F. Vito 1, 00168, Rome, Italy.
Stefano SignorettiDivision of Neurosurgery, Department of Neurosciences Head and Neck Surgery, S. Camillo Hospital, Circonvallazione Gianicolense 87, 00152, Rome, Italy.
Lisa J HillNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK.
Edoardo PortoNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK.
Barbara TavazziInstitute of Biochemistry and Clinical Biochemistry, Catholic University of Rome, Largo F. Vito 1, 00168, Rome, Italy. barbara.tavazzi@unicatt.it.
Giuseppe LazzarinoDepartment of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Viale A. Doria 6, 95125, Catania, Italy. lazzarig@unict.it.ORCID 0000-0002-5917-7279
Antonio BelliNeuroscience and Ophthalmology Research Group, Institute of Inflammation and Ageing, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, B15 2TT, Birmingham, UK.
Università Cattolica del Sacro Cuore · ITNational Institute for Health Research · GBIRCCS San Camillo Hospital · ITUniversity of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dynamics are regulated by a complex system of proteins representing the mitochondrial quality control (MQC). MQC balances antagonistic forces of fusion and fission determining mitochondrial and cell fates. In several neurological disorders, dysfunctional mitochondria show significant changes in gene and protein expression of the MQC and contribute to the pathophysiological mechanisms of cell damage. In this study, we evaluated the main gene and protein expression involved in the MQC in rats receiving traumatic brain injury (TBI) of different severities. At 6, 24, 48 and 120 hours after mild TBI (mTBI) or severe TBI (sTBI), gene and protein expressions of fusion and fission were measured in brain tissue homogenates. Compared to intact brain controls, results showed that genes and proteins inducing fusion or fission were upregulated and downregulated, respectively, in mTBI, but downregulated and upregulated, respectively, in sTBI. In particular, OPA1, regulating inner membrane dynamics, cristae remodelling, oxidative phosphorylation, was post-translationally cleaved generating differential amounts of long and short OPA1 in mTBI and sTBI. Corroborated by data referring to citrate synthase, these results confirm the transitory (mTBI) or permanent (sTBI) mitochondrial dysfunction, enhancing MQC importance to maintain cell functions and indicating in OPA1 an attractive potential therapeutic target for TBI.

Indexed as

Mitochondrial DynamicsAnimalsBiomarkersBrainBrain Injuries, TraumaticGene Expression ProfilingGene Expression RegulationMaleMitochondriaMitophagyRatsSeverity of Illness IndexBiomarkers

Identifiers

PMID28835707
PMCPMC5569027
OpenAlexW2749314878

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.