Evidence map›Paper›PMID 40712573›Full record

ArticleCell reports. Medicine2025

Opantimirs: A class of antagonizing microRNAs that upregulate Opa1 and improve mitochondrial and disuse myopathies.

Andre Djalalvandi, Keisuke Takeda, Francesca Grespi, Hualin Fan, Tiago Branco Fonseca, Leonardo Nogara, Saman Sharifi, Carlotta Barison, Martina Semenzato, Akiko Omori and 9 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

19 authors.

Andre DjalalvandiDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Keisuke TakedaDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Francesca GrespiDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Hualin FanDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Tiago Branco FonsecaDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Leonardo NogaraVeneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biomedical Sciences University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Department of Pharmaceutical Sciences, University of Padova, Via Marzolo, 5 35131 Padova, Italy.
Saman SharifiVeneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Medicine, University of Padova, Via Giustininani 1, 35128 Padova, Italy.
Carlotta BarisonDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Martina SemenzatoDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Akiko OmoriDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Raffaele CeruttiVeneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biomedical Sciences University of Padova, Via U. Bassi 58B, 35121 Padova, Italy.
Davide SteffanVeneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biomedical Sciences University of Padova, Via U. Bassi 58B, 35121 Padova, Italy.
Lorenza TsansiziDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Valeria BalmacedaDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Lukas AlanDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Camilla BeanDepartment of Medical Sciences, University of Udine, Via Colugna 50, 33100 Udine, Italy.
Bert BlaauwVeneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biomedical Sciences University of Padova, Via U. Bassi 58B, 35121 Padova, Italy.
Carlo ViscomiVeneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biomedical Sciences University of Padova, Via U. Bassi 58B, 35121 Padova, Italy.
Luca ScorranoDepartment of Biology, University of Padova, Via U. Bassi 58B, 35121 Padova, Italy; Veneto Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy. Electronic address: luca.scorrano@unipd.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in mitochondrial ultrastructure and reduced levels of the crista-shaping protein Opa1 are key features of mitochondrial myopathies and aging. We identify and characterize a biological therapy that improves mitochondrial and disuse myopathy models by boosting Opa1 levels. In silico analysis identifies microRNAs (miRNAs) 128-3p and 148/152-3p family as conserved modulators of OPA1 transcription and elevated in various muscle disorders. These miRNAs target the 3' UTR of murine and human OPA1, reducing its mRNA and protein levels, causing mitochondrial fragmentation and crista disorganization. Genetic experiments confirm that their mitochondrial effects rely on 3' UTR binding. In mitochondrial disease patient cells and murine models, elevated OPA1-specific miRNA levels are reduced by antagonistic miRNAs (Opantimirs), which restore mitochondrial ultrastructure, morphology, and function. In vivo, Opantimirs correct mitochondrial ultrastructure and fiber size in muscles of denervated and Cox15-ablated mice, improving strength in the latter. Thus, biopharmacological correction of the mitochondrial ultrastructure can ameliorate mitochondrial myopathies.

Indexed as

GTP PhosphohydrolasesMicroRNAsMitochondriaMitochondrial MyopathiesUp-Regulation3' Untranslated RegionsAnimalsDisease Models, AnimalHumansMiceMuscle, Skeletal3' Untranslated RegionsGTP PhosphohydrolasesMicroRNAsOPA1 protein, humanOpa1 protein, mouseantimiRscristae remodelingdisuse myopathiesmicroRNAsmiR-128-3pmiR-148/152-3p familymitochondrial myopathiesmitochondrial ultrastructureOPA1

Identifiers

PMID40712573
PMCPMC12432375

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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.