Evidence map›Paper›PMID 38334639›Full record

ReviewCells2024

Mitochondria: A Promising Convergent Target for the Treatment of Amyotrophic Lateral Sclerosis.

Teresa Cunha-Oliveira, Liliana Montezinho, Rui F Simões, Marcelo Carvalho, Elisabete Ferreiro, Filomena S G Silva

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

22 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  3. CTRP1 regulates skeletal muscle differentiation through quality control of mitochondrial dynamics and function.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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  14. [A portable steady-state visual evoked potential brain-computer interface system for smart healthcare].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2025
    Article
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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 3 institutions in 1 country.

Teresa Cunha-OliveiraCNC-Center for Neuroscience and Cell Biology, CIBB-Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504 Coimbra, Portugal.ORCID 0000-0002-7382-0339
Liliana MontezinhoCenter for Investigation Vasco da Gama (CIVG), Escola Universitária Vasco da Gama, 3020-210 Coimbra, Portugal.ORCID 0000-0002-6877-4286
Rui F SimõesCNC-Center for Neuroscience and Cell Biology, CIBB-Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504 Coimbra, Portugal.
Marcelo CarvalhoCNC-Center for Neuroscience and Cell Biology, CIBB-Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504 Coimbra, Portugal.
Elisabete FerreiroCNC-Center for Neuroscience and Cell Biology, CIBB-Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504 Coimbra, Portugal.ORCID 0000-0002-1200-4602
Filomena S G SilvaCNC-Center for Neuroscience and Cell Biology, CIBB-Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504 Coimbra, Portugal.ORCID 0000-0001-7143-8905
University of Coimbra · PTBiocant · PTEscola Universitária Vasco da Gama · PT

Funding

Fundação para a Ciência e Tecnologia 2022.00011.CEECINDFundação para a Ciência e Tecnologia CEECIND/00322/2017Fundação para a Ciência e Tecnologia DL57/2016/CP1448/CT0016Fundação para a Ciência e Tecnologia POCI-01-0145-FEDER-029297Fundação para a Ciência e Tecnologia POCI-01-0145-FEDER-029391Fundação para a Ciência e Tecnologia PTDC/BTM-ORG/0055/2021Fundação para a Ciência e Tecnologia PTDC/BTM-SAL/29297/2017Fundação para a Ciência e Tecnologia PTDC/MED-FAR/29391/2017Fundação para a Ciência e Tecnologia UIDB/00081/2020Fundação para a Ciência e Tecnologia UIDB/04539/2020Fundação para a Ciência e Tecnologia UIDP/04539/2020
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by the progressive loss of motor neurons, for which current treatment options are limited. Recent studies have shed light on the role of mitochondria in ALS pathogenesis, making them an attractive therapeutic intervention target. This review contains a very comprehensive critical description of the involvement of mitochondria and mitochondria-mediated mechanisms in ALS. The review covers several key areas related to mitochondria in ALS, including impaired mitochondrial function, mitochondrial bioenergetics, reactive oxygen species, metabolic processes and energy metabolism, mitochondrial dynamics, turnover, autophagy and mitophagy, impaired mitochondrial transport, and apoptosis. This review also highlights preclinical and clinical studies that have investigated various mitochondria-targeted therapies for ALS treatment. These include strategies to improve mitochondrial function, such as the use of dichloroacetate, ketogenic and high-fat diets, acetyl-carnitine, and mitochondria-targeted antioxidants. Additionally, antiapoptotic agents, like the mPTP-targeting agents minocycline and rasagiline, are discussed. The paper aims to contribute to the identification of effective mitochondria-targeted therapies for ALS treatment by synthesizing the current understanding of the role of mitochondria in ALS pathogenesis and reviewing potential convergent therapeutic interventions. The complex interplay between mitochondria and the pathogenic mechanisms of ALS holds promise for the development of novel treatment strategies to combat this devastating disease.

Indexed as

Amyotrophic Lateral SclerosisNeurodegenerative DiseasesApoptosisHumansMitochondriaMotor Neuronsamyotrophic lateral sclerosismitochondrial dysfunctionmitochondria-targeted therapiesmotor neuron degenerationneurodegenerationpathological mechanismstherapeutic interventions

Identifiers

PMID38334639
PMCPMC10854804
OpenAlexW4391315130

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.