Evidence map›Paper›PMID 26039448›Full record

ArticleCell metabolism2015

The OPA1-dependent mitochondrial cristae remodeling pathway controls atrophic, apoptotic, and ischemic tissue damage.

Tatiana Varanita, Maria Eugenia Soriano, Vanina Romanello, Tania Zaglia, Rubén Quintana-Cabrera, Martina Semenzato, Roberta Menabò, Veronica Costa, Gabriele Civiletto, Paola Pesce and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 279 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
279citing papers in PubMed, 1 pooled it
20.8field-weighted citation impact, top 1% 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

279 citing papers in PubMed, 1 synthesis or guideline pooled it, 444 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD.bioRxiv : the preprint server for biology · 2026
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  9. Specific FbioRxiv : the preprint server for biology · 2026
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  19. Multiscale mitochondrial cristae remodeling links Opa1 downregulation to reduced OXPHOS capacity in aged hearts.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  20. Article

219 more citing papers are in PubMed but not listed here.

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

16 authors at 5 institutions in 2 countries.

Tatiana VaranitaDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biology, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Maria Eugenia SorianoDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biology, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Vanina RomanelloDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biomedical Sciences, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Tania ZagliaDepartment of Biomedical Sciences, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Rubén Quintana-CabreraDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biology, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Martina SemenzatoDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biology, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Roberta MenabòInstitute of Neuroscience, National Research Council of Italy (CNR), Via C. Colombo 3, 35121 Padova, Italy.
Veronica CostaDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy.
Gabriele CivilettoFondazione IRCCS Istituto Neurologico "C. Besta," Via L. Temolo 4, 20126 Milan, Italy; MRC Mitochondrial Biology Unit, MRC Building, Hills Road, Cambridge CB2 0XY, UK.
Paola PesceDepartment of Cardiac, Thoracic and Vascular Sciences, University of Padova, Via Giustiniani, 2, 35128 Padova, Italy.
Carlo ViscomiFondazione IRCCS Istituto Neurologico "C. Besta," Via L. Temolo 4, 20126 Milan, Italy; MRC Mitochondrial Biology Unit, MRC Building, Hills Road, Cambridge CB2 0XY, UK.
Massimo ZevianiFondazione IRCCS Istituto Neurologico "C. Besta," Via L. Temolo 4, 20126 Milan, Italy; MRC Mitochondrial Biology Unit, MRC Building, Hills Road, Cambridge CB2 0XY, UK.
Fabio Di LisaDepartment of Biomedical Sciences, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Marco MongilloDepartment of Biomedical Sciences, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Marco SandriDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biomedical Sciences, University of Padova, Via C. Colombo 3, 35121 Padova, Italy.
Luca ScorranoDulbecco Telethon Institute, Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padova, Italy; Department of Biology, University of Padova, Via C. Colombo 3, 35121 Padova, Italy. Electronic address: luca.scorrano@unipd.it.
University of Padua · ITDulbecco Telethon Institute · ITFondazione IRCCS Istituto Neurologico Carlo Besta · ITVeneto Institute of Molecular Medicine · ITNational Research Council · IT

Funding

Medical Research Council MC_UP_1002/1Telethon GGP12162Telethon GGP14187Telethon GPP10005
6 · The paper itself

Abstract

Mitochondrial morphological and ultrastructural changes occur during apoptosis and autophagy, but whether they are relevant in vivo for tissue response to damage is unclear. Here we investigate the role of the optic atrophy 1 (OPA1)-dependent cristae remodeling pathway in vivo and provide evidence that it regulates the response of multiple tissues to apoptotic, necrotic, and atrophic stimuli. Genetic inhibition of the cristae remodeling pathway in vivo does not affect development, but protects mice from denervation-induced muscular atrophy, ischemic heart and brain damage, as well as hepatocellular apoptosis. Mechanistically, OPA1-dependent mitochondrial cristae stabilization increases mitochondrial respiratory efficiency and blunts mitochondrial dysfunction, cytochrome c release, and reactive oxygen species production. Our results indicate that the OPA1-dependent cristae remodeling pathway is a fundamental, targetable determinant of tissue damage in vivo.

Indexed as

Oxygen ConsumptionAnimalsCytochromes cGTP PhosphohydrolasesMiceMice, TransgenicMitochondriaMuscular AtrophyReactive Oxygen SpeciesCytochromes cGTP PhosphohydrolasesOpa1 protein, mouseReactive Oxygen Species

Identifiers

PMID26039448
PMCPMC4457892
OpenAlexW1570973990

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.