Evidence map›Paper›PMID 42651639›Full record

ArticleBiology2026

Targeting Mitochondrial Fission Produces Both Neuroprotective and Detrimental Effects in the SOD1 Mouse Model of Amyotrophic Lateral Sclerosis.

Maria Ciuro, Chantal Rovetto, Angela A Sirna, Salvatore Giunta, Giampiero Leanza, Rosario Gulino

Abstract read
In one paragraph

Article in Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Maria CiuroDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 89, 95123 Catania, Italy.
Chantal RovettoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 89, 95123 Catania, Italy.
Angela A SirnaDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 89, 95123 Catania, Italy.
Salvatore GiuntaDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 89, 95123 Catania, Italy.ORCID 0000-0002-8095-8678
Giampiero LeanzaDepartment of Drug and Health Sciences, University of Catania, Via Santa Sofia 64, 95125 Catania, Italy.ORCID 0000-0002-8609-2561
Rosario GulinoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 89, 95123 Catania, Italy.ORCID 0000-0002-8067-697X

Funding

Fondazione Italiana di Ricerca per la Sclerosi Laterale Amiotrofica PG_6/2022
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neuromuscular disease characterized by progressive motor neuron (MN) degeneration and severe skeletal muscle atrophy. Despite extensive research, the mechanisms driving disease onset and progression remain incompletely understood. While MN loss is a defining feature of ALS, increasing evidence indicates that mitochondrial dysfunction contributes to disease pathogenesis. Here, we investigated the hypothesis that Mdivi-1, a pharmacological inhibitor of mitochondrial fission protein Drp-1, may exert neuroprotective properties in the SOD1

Indexed as

amyotrophic lateral sclerosisdynamin-related protein 1Mdivi-1mitochondrial dynamicsmotor neuronsphysiologyskeletal muscle atrophySOD1G93A mouse modelsynaptic plasticityTAR DNA-binding protein 43

Identifiers

PMID42651639
PMCPMC13510057

What OpenQuestion holds

Textmetadata
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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.