Evidence map›Paper›PMID 40653481›Full record

ArticleActa neuropathologica communications2025

Kv3 channel agonist ameliorates the phenotype of a mouse model of amyotrophic lateral sclerosis.

Manuela Marabita, Caterina Marchioretti, Aishwarya Aravamudhan, Simona Zito, Antonella Falconieri, Emanuela Zuccaro, Roberta Andreotti, Lisa Gambarotto, Samuele Metti, Marika Tonellato and 19 more

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. KFrontiers in pharmacology · 2026
    Pooled it
  2. Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  3. Article
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

29 authors.

Manuela Marabita *BioTiChe Drug Discovery, Istituto di Ricerca Pediatrica Città della Speranza, Padova, 35127, Italy.
Caterina Marchioretti *Department of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Aishwarya Aravamudhan *Department of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Simona ZitoDepartment of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Antonella FalconieriDepartment of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Emanuela ZuccaroDepartment of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Roberta AndreottiDepartment of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Lisa GambarottoDepartment of Molecular Medicine (DMM), University of Padova, Padova, 35131, Italy.
Samuele MettiDepartment of Molecular Medicine (DMM), University of Padova, Padova, 35131, Italy.
Marika TonellatoDepartment of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Valentina AdamiBioTiChe Drug Discovery, Istituto di Ricerca Pediatrica Città della Speranza, Padova, 35127, Italy.
Kyung Ho ParkNaason Science Inc, Saengmyung-Ro 123, Osong-eup, Heungdeok-gu, Cheongju-si, Chungbuk, 28160, Korea.
Martin J GunthorpeAutifony Therapeutics, Ltd, Stevenage Bioscience Catalyst, Gunnels Wood Road, Stevenage, SG1 2FX, UK.
Charles H LargeAutifony Therapeutics, Ltd, Stevenage Bioscience Catalyst, Gunnels Wood Road, Stevenage, SG1 2FX, UK.
Agostino MarascoBioTiChe Drug Discovery, Istituto di Ricerca Pediatrica Città della Speranza, Padova, 35127, Italy.
Sara VianelloDepartment of Neuroscience (DNS), Neuromuscular Center, University of Padova, Padova, 35128, Italy.
Jessica RosatiCellular Reprogramming Unit, Fondazione IRCCS Casa Sollievo della Sofferenza, Foggia, 71100, Italy.
Elisa BelluzziDepartment of Orthopaedics and Orthopaedic Oncology, Department of Surgery, Oncology, and Gastroenterology (DiSCOG), University-Hospital of Padova, Padova, 35128, Italy.
Assunta PozzuoliDepartment of Orthopaedics and Orthopaedic Oncology, Department of Surgery, Oncology, and Gastroenterology (DiSCOG), University-Hospital of Padova, Padova, 35128, Italy.
Carlo BizDepartment of Orthopaedics and Orthopaedic Oncology, Department of Surgery, Oncology, and Gastroenterology (DiSCOG), University-Hospital of Padova, Padova, 35128, Italy.
Pietro RuggieriDepartment of Orthopaedics and Orthopaedic Oncology, Department of Surgery, Oncology, and Gastroenterology (DiSCOG), University-Hospital of Padova, Padova, 35128, Italy.
Manuela BassoDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, Trento, 38123, Italy.
Angelo PolettiDepartment of Biomolecular and Pharmacological Sciences Rodolfo Paoletti, University of Milan, Milan, 20133, Italy.
Giuseppe AlvaroBioTiChe Drug Discovery, Istituto di Ricerca Pediatrica Città della Speranza, Padova, 35127, Italy.
Gianni SorarùDepartment of Neuroscience (DNS), Neuromuscular Center, University of Padova, Padova, 35128, Italy.
Paolo BonaldoDepartment of Molecular Medicine (DMM), University of Padova, Padova, 35131, Italy.
Ornella RossettoDepartment of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy.
Nadia PilatiBioTiChe Drug Discovery, Istituto di Ricerca Pediatrica Città della Speranza, Padova, 35127, Italy. nadia.pilati@biotiche.com.
Maria PennutoDepartment of Biomedical Sciences (DBS), University of Padova, Padova, 35131, Italy. maria.pennuto@unipd.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Voltage-gated potassium channels, Kv3.1, Kv3.2, Kv3.3, and Kv3.4, facilitate rapid repolarization and shape action potentials, which are crucial to maintaining high-frequency firing. Little is known about the expression and function of Kv3 channels in skeletal muscle. We show that these channels are expressed in type IIa/IIx fibers, and their transcript levels progressively increase from postnatal age to adulthood in physiological context. In mature myofibers, the Kv3.1 and Kv3.4 channels are enriched in the muscle triads. The expression of the Kv3 channel is lost upon acute motor unit damage, in mouse models of amyotrophic lateral sclerosis (ALS) and spinal and bulbar muscular atrophy (SBMA), and the skeletal muscle of patients with sporadic ALS. Early treatment of ALS and SBMA mice with AUT00201, a positive allosteric modulator of Kv3 channels, improved the phenotype of ALS mice specifically, suggesting that positive modulation of Kv3 channels is a novel therapeutic option for patients with ALS.

Indexed as

Amyotrophic Lateral SclerosisShaw Potassium ChannelsAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMice, TransgenicMuscle, SkeletalPhenotypeSuperoxide Dismutase-1Shaw Potassium ChannelsSuperoxide Dismutase-1

Identifiers

PMID40653481
PMCPMC12257725

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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.