Evidence map›Paper›PMID 28483998›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Hypoxia treatment reverses neurodegenerative disease in a mouse model of Leigh syndrome.

Michele Ferrari, Isha H Jain, Olga Goldberger, Emanuele Rezoagli, Robrecht Thoonen, Kai-Hung Cheng, David E Sosnovik, Marielle Scherrer-Crosbie, Vamsi K Mootha, Warren M Zapol

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

110 citing papers in PubMed, 165 citations in OpenAlex.

  1. Review
  2. A second-generation "hypoxia in a pill" rescues neurodegenerative phenotypes across distinct mouse models.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
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  6. Article
  7. Review
  8. Article
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  15. Power and poison: The intersections of HThe Journal of biological chemistry · 2025
    Review
  16. Article
  17. Therapies for Mitochondrial Disease: Past, Present, and Future.Journal of inherited metabolic disease · 2025
    Review
  18. Respiratory complex IIIbioRxiv : the preprint server for biology · 2025
    Article
  19. Review
  20. Hypoxia in multiple sclerosis.Redox biology · 2025
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Michele FerrariDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114.
Isha H JainDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114.
Olga GoldbergerDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114.
Emanuele RezoagliDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114.
Robrecht ThoonenCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114.
Kai-Hung ChengCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114.
David E SosnovikCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114.
Marielle Scherrer-CrosbieCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114.
Vamsi K MoothaDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114; vamsi@hms.harvard.edu wzapol@mgh.harvard.edu.
Warren M ZapolDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114; vamsi@hms.harvard.edu wzapol@mgh.harvard.edu.
Massachusetts General Hospital · USBroad Institute · USHoward Hughes Medical Institute · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

The most common pediatric mitochondrial disease is Leigh syndrome, an episodic, subacute neurodegeneration that can lead to death within the first few years of life, for which there are no proven general therapies. Mice lacking the complex I subunit, Ndufs4, develop a fatal progressive encephalopathy resembling Leigh syndrome and die at ≈60 d of age. We previously reported that continuously breathing normobaric 11% O

Indexed as

AnimalsDisease Models, AnimalElectron Transport Complex IHypoxiaLeigh DiseaseMiceMice, Inbred C57BLMice, KnockoutMitochondriaNeurodegenerative DiseasesOxygenRespirationElectron Transport Complex INdufs4 protein, mouseOxygenhypoxiaLeigh syndromemitochondrianeurodegenerationoxygen

Identifiers

PMID28483998
PMCPMC5448167
OpenAlexW2612960139

What OpenQuestion holds

Textmetadata
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.