Evidence map›Paper›PMID 35092170›Full record

ArticleThe FEBS journal2022

The mitochondrial protein Sideroflexin 3 (SFXN3) influences neurodegeneration pathways in vivo.

Leire M Ledahawsky, Maria Eirini Terzenidou, Ruairidh Edwards, Rachel A Kline, Laura C Graham, Samantha L Eaton, Dinja van der Hoorn, Helena Chaytow, Yu-Ting Huang, Ewout J N Groen and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The FEBS journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Peptide Electrostatic Modulation Directs Human Neural Cell Fate.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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

15 authors at 3 institutions in 2 countries.

Leire M LedahawskyEdinburgh Medical School, Biomedical Sciences, University of Edinburgh, UK.
Maria Eirini TerzenidouInstitute of Molecular Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, UK.
Ruairidh EdwardsInstitute of Molecular Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, UK.
Rachel A KlineEuan MacDonald Centre for Motor Neuron Disease Research, University of Edinburgh, UK.
Laura C GrahamEuan MacDonald Centre for Motor Neuron Disease Research, University of Edinburgh, UK.
Samantha L EatonEuan MacDonald Centre for Motor Neuron Disease Research, University of Edinburgh, UK.
Dinja van der HoornEdinburgh Medical School, Biomedical Sciences, University of Edinburgh, UK.
Helena ChaytowEdinburgh Medical School, Biomedical Sciences, University of Edinburgh, UK.
Yu-Ting HuangEdinburgh Medical School, Biomedical Sciences, University of Edinburgh, UK.
Ewout J N GroenEdinburgh Medical School, Biomedical Sciences, University of Edinburgh, UK.ORCID 0000-0002-2330-9444
Anna A L MotylEdinburgh Medical School, Biomedical Sciences, University of Edinburgh, UK.
Douglas J LamontFingerPrints Proteomics Facility, University of Dundee, UK.
Kostas TokatlidisInstitute of Molecular Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, UK.
Thomas M WishartEuan MacDonald Centre for Motor Neuron Disease Research, University of Edinburgh, UK.
Thomas H GillingwaterEdinburgh Medical School, Biomedical Sciences, University of Edinburgh, UK.ORCID 0000-0002-0306-5577
Mott MacDonald (United Kingdom) · GBUniversity of Glasgow · GBUniversity of Dundee · GB

Funding

Biotechnology and Biological Sciences Research Council BB/R009031/1Biotechnology and Biological Sciences Research Council BBS/E/D/20251969Biotechnology and Biological Sciences Research Council BB/T003804/1Medical Research Council MC_PC_16043Medical Research Council MC_PC_17190Medical Research Council MC_PC_18048Medical Research Council MC_PC_19039
6 · The paper itself

Abstract

Synapses are a primary pathological target in neurodegenerative diseases. Identifying therapeutic targets at the synapse could delay progression of numerous conditions. The mitochondrial protein SFXN3 is a neuronally enriched protein expressed in synaptic terminals and regulated by key synaptic proteins, including α-synuclein. We first show that SFXN3 uses the carrier import pathway to insert into the inner mitochondrial membrane. Using high-resolution proteomics on Sfxn3-KO mice synapses, we then demonstrate that SFXN3 influences proteins and pathways associated with neurodegeneration and cell death (including CSPα and Caspase-3), as well as neurological conditions (including Parkinson's disease and Alzheimer's disease). Overexpression of SFXN3 orthologues in Drosophila models of Parkinson's disease significantly reduced dopaminergic neuron loss. In contrast, the loss of SFXN3 was insufficient to trigger neurodegeneration in mice, indicating an anti- rather than pro-neurodegeneration role for SFXN3. Taken together, these results suggest a potential role for SFXN3 in the regulation of neurodegeneration pathways.

Indexed as

Cation Transport Proteinsalpha-SynucleinAnimalsMiceMitochondrial MembranesMitochondrial ProteinsNerve DegenerationParkinson DiseaseSynapsesalpha-SynucleinCation Transport ProteinsMitochondrial ProteinsSfxn3 protein, mousemitochondrianeurodegenerationParkinson's diseaseSideroflexin 3synapse

Identifiers

PMID35092170
PMCPMC9542548
OpenAlexW4210540567

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.