Evidence map›Paper›PMID 28110471›Full record

ArticleMolecular neurobiology2018

Depletion of Mitofusin-2 Causes Mitochondrial Damage in Cisplatin-Induced Neuropathy.

Ilja Bobylev, Abhijeet R Joshi, Mohammed Barham, Wolfram F Neiss, Helmar C Lehmann

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Oxaliplatin-induced peripheral neuropathy: from pathogenesis to treatment.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Protective effects ofVeterinary research forum : an international quarterly journal · 2022
    Article
  10. Article
  11. Review
  12. Review
  13. Chemotherapy and peripheral neuropathy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review
  14. Review
  15. Review
  16. Early Physiological and Cellular Indicators of Cisplatin-Induced Ototoxicity.Journal of the Association for Research in Otolaryngology : JARO · 2021
    Article
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Ilja BobylevDepartment of Neurology, University Hospital of Cologne, Cologne, Germany.
Abhijeet R JoshiDepartment of Neurology, University Hospital of Cologne, Cologne, Germany.
Mohammed BarhamDepartment of Anatomy I, Medical Faculty, University of Cologne, Cologne, Germany.
Wolfram F NeissDepartment of Anatomy I, Medical Faculty, University of Cologne, Cologne, Germany.
Helmar C LehmannDepartment of Neurology, University Hospital of Cologne, Cologne, Germany. helmar.lehmann@uk-koeln.de.
University of Cologne · DEUniversity Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sensory neuropathy is a relevant side effect of the antineoplastic agent cisplatin. Mitochondrial damage is assumed to play a critical role in cisplatin-induced peripheral neuropathy, but the pathomechanisms underlying cisplatin-induced mitotoxicity and neurodegeneration are incompletely understood. In an animal model of cisplatin-induced neuropathy, we determined in detail the extent and spatial distribution of mitochondrial damage during cisplatin treatment. Changes in the total number of axonal mitochondria during cisplatin treatment were assessed in intercostal nerves from transgenic mice that express cyan fluorescent protein. Further, we explored the impact of cisplatin on the expression of nuclear encoded molecules of mitochondrial fusion and fission, including mitofusin-2 (MFN2), optic atrophy 1 (OPA1), and dynamin-related protein 1 (DRP1). Cisplatin treatment resulted in a loss of total mitochondrial mass in axons and in an abnormal mitochondrial morphology including atypical enlargement, increased vacuolization, and loss of cristae. These changes were observed in distal and proximal nerve segments and were more prominent in axons than in Schwann cells. Transcripts of fusion and fission proteins were reduced in distal nerve segments. Significant reduced expression levels of the fusion protein MFN2 was detected in nerves of cisplatin-exposed animals. In summary, we provide for the first time an evidence that cisplatin alters mitochondrial dynamics in peripheral nerves. Loss of MFN2, previously implicated in the pathogenesis of other neurodegenerative diseases, also contributes to the pathogenesis in cisplatin-induced neuropathy.

Indexed as

AnimalsAntineoplastic AgentsCisplatinDisease Models, AnimalDynaminsGTP PhosphohydrolasesMiceMice, TransgenicMitochondriaMitochondrial DynamicsPeripheral Nervous System DiseasesSchwann CellsSciatic NerveAntineoplastic AgentsCisplatinDnm1l protein, mouseDynaminsGTP PhosphohydrolasesMfn2 protein, mouseOpa1 protein, mouseCIPNCisplatin neurotoxicityDRGFusion and fissionMitochondria

Identifiers

PMID28110471
OpenAlexW2577605944

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.