Evidence map›Paper›PMID 30979712›Full record

ArticleEMBO molecular medicine2019

miR-181a/b downregulation exerts a protective action on mitochondrial disease models.

Alessia Indrieri, Sabrina Carrella, Alessia Romano, Alessandra Spaziano, Elena Marrocco, Erika Fernandez-Vizarra, Sara Barbato, Mariateresa Pizzo, Yulia Ezhova, Francesca M Golia and 10 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Review
  3. Uncovering mitochondrial defects in photoreceptors opens therapeutic opportunities for Stargardt disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
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  7. Gene therapy and mRNA drugs approach for mitochondrial OXPHOS deficiencies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  8. Article
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  10. Molecular therapy. Nucleic acids · 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

20 authors at 6 institutions in 3 countries.

Alessia IndrieriTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.ORCID 0000-0002-2325-0913
Sabrina CarrellaTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Alessia RomanoTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Alessandra SpazianoTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Elena MarroccoTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Erika Fernandez-VizarraMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.ORCID 0000-0002-2469-142X
Sara BarbatoTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Mariateresa PizzoTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Yulia EzhovaTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Francesca M GoliaTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Ludovica CiampiTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Roberta TammaroTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Jorge Henao-MejiaDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Adam WilliamsThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Richard A FlavellDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
Elvira De LeonibusTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Massimo ZevianiMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.ORCID 0000-0002-9067-5508
Enrico M SuraceTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Sandro BanfiTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy banfi@tigem.it franco@tigem.it.ORCID 0000-0002-6541-8833
Brunella FrancoTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy banfi@tigem.it franco@tigem.it.ORCID 0000-0001-5588-4569
Telethon Institute Of Genetics And Medicine · ITUniversity of Cambridge · GBUniversity of Campania "Luigi Vanvitelli" · ITHoward Hughes Medical Institute · USJackson Laboratory · USUniversity of Pennsylvania · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Regulation of short-lived myeloid cells by the novel long non-coding RNA MorrbidR01HL136572 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI HENAO-MEJIA, JORGE · 2017 to 2021
$2.0M
Medical Research Council MC_EX_MR/P007031/1Medical Research Council MC_UP_1002/1Medical Research Council MC_UU_00015/5Medical Research Council MC_UU_00015/7Medical Research Council MC_UU_00015/8MRF_ MRF-155-0001-S-MARTIMRF_ MRF-155-0002-RG-ZEVIAMRF_ MRF-155-0005-RG-ZEVI-C0784NCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL136572
6 · The paper itself

Abstract

Mitochondrial diseases (MDs) are a heterogeneous group of devastating and often fatal disorders due to defective oxidative phosphorylation. Despite the recent advances in mitochondrial medicine, effective therapies are still not available for these conditions. Here, we demonstrate that the microRNAs miR-181a and miR-181b (miR-181a/b) regulate key genes involved in mitochondrial biogenesis and function and that downregulation of these miRNAs enhances mitochondrial turnover in the retina through the coordinated activation of mitochondrial biogenesis and mitophagy. We thus tested the effect of miR-181a/b inactivation in different animal models of MDs, such as microphthalmia with linear skin lesions and Leber's hereditary optic neuropathy. We found that miR-181a/b downregulation strongly protects retinal neurons from cell death and significantly ameliorates the disease phenotype in all tested models. Altogether, our results demonstrate that miR-181a/b regulate mitochondrial homeostasis and that these miRNAs may be effective gene-independent therapeutic targets for MDs characterized by neuronal degeneration.

Indexed as

AnimalsAutophagyCell DeathCell LineCytoprotectionDisease Models, AnimalDown-RegulationElectron Transport Complex IFemaleHumansMaleMiceMicroRNAsMitochondriaMitochondrial DiseasesMitochondrial DynamicsElectron Transport Complex IMicroRNAsMIrn181 microRNA, humanmirn181 microRNA, mouseNdufs4 protein, mouseLHONmicroRNAmiR‐181mitochondrial diseaseneurodegeneration

Identifiers

PMID30979712
PMCPMC6505685
OpenAlexW2936777020

What OpenQuestion holds

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LicenceCC BY
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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.