Evidence map›Paper›PMID 28842714›Full record

ArticleScientific reports2017

Potential therapeutic targets for ALS: MIR206, MIR208b and MIR499 are modulated during disease progression in the skeletal muscle of patients.

Lorena Di Pietro, Mirko Baranzini, Maria Grazia Berardinelli, Wanda Lattanzi, Mauro Monforte, Giorgio Tasca, Amelia Conte, Giandomenico Logroscino, Fabrizio Michetti, Enzo Ricci and 2 more

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 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Exploring dysregulated miRNAs in ALS: implications for disease pathogenesis and early diagnosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  16. The Cellular and Molecular Signature of ALS in Muscle.Journal of personalized medicine · 2022
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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

12 authors at 3 institutions in 1 country.

Lorena Di PietroInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy.
Mirko BaranziniInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy.
Maria Grazia BerardinelliInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy.
Wanda LattanziInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy.
Mauro MonforteInstitute of Neurology, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario "A. Gemelli", 00168, Rome, Italy.
Giorgio TascaInstitute of Neurology, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario "A. Gemelli", 00168, Rome, Italy.
Amelia ConteNEuroMuscularOmnicentre (NEMO), Fondazione Serena Onlus, 00168, Rome, Italy.
Giandomenico LogroscinoInstitute of Orthopedic Clinic, Fondazione Policlinico Universitario "A. Gemelli", 00168, Rome, Italy.
Fabrizio MichettiInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy.
Enzo RicciInstitute of Neurology, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario "A. Gemelli", 00168, Rome, Italy.
Mario SabatelliInstitute of Neurology, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario "A. Gemelli", 00168, Rome, Italy.
Camilla BernardiniInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, 00168, Rome, Italy. camilla.bernardini@unicatt.it.
Università Cattolica del Sacro Cuore · ITCentro Clinico Nemo · ITAgostino Gemelli University Polyclinic · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is characterized by the progressive loss of motor neurons followed by muscle weakness, paralysis and death. The disease progression is extremely variable among patients, and reliable prognostic markers have not been identified. The aim of the study was to functionally characterize selected genes and microRNAs acting in the skeletal muscle of ALS patients, taking into account the duration and evolution of the disease, in order to obtain information regarding the muscle response to ALS progression. This prospective, longitudinal study enrolled 14 ALS patients and 24 age- and sex-matched healthy controls. Gene expression and histological analysis indicated an increase of MIR208B and MIR499 levels and the predominance of slow fibres, respectively, in the muscles of patients with a slower disease progression. A decreased expression of MIR206 and increased levels of HDAC4, during the progression of the disease were also observed. Taken together, our data suggest that the molecular signalling that regulates re-innervation and muscle regeneration is hampered during the progression of skeletal muscle impairment in ALS. This could provide precious hints towards defining prognostic protocols, and designing novel tailored therapeutic approaches, to improve ALS patients' care and delay disease progression.

Indexed as

AdultAgedAmyotrophic Lateral SclerosisBiomarkersBiopsyCell DifferentiationDisease ProgressionFemaleGene Expression ProfilingGene Expression RegulationHumansMaleMicroRNAsMiddle AgedMolecular Targeted TherapyMuscle DevelopmentBiomarkersMicroRNAsMIRN206 microRNA, humanMIRN208 microRNA, humanMIRN499 microRNA, human

Identifiers

PMID28842714
PMCPMC5573384
OpenAlexW2747461216

What OpenQuestion holds

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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.