Evidence map›Paper›PMID 33207782›Full record

ArticleInternational journal of molecular sciences2020

Platinum-Based Drugs Cause Mitochondrial Dysfunction in Cultured Dorsal Root Ganglion Neurons.

Markus Leo, Linda-Isabell Schmitt, Patricia Küsterarent, Andrea Kutritz, Tienush Rassaf, Christoph Kleinschnitz, Ulrike B Hendgen-Cotta, Tim Hagenacker

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

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  17. Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
    Review
  18. Soluble epoxide hydrolase inhibition alleviates chemotherapy induced neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
    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

8 authors at 1 institution in 1 country.

Markus LeoDepartment of Neurology, NeuroScienceLab, Medical Faculty, University Medicine Essen, 45147 Essen, Germany.
Linda-Isabell SchmittDepartment of Neurology, NeuroScienceLab, Medical Faculty, University Medicine Essen, 45147 Essen, Germany.
Patricia KüsterarentDepartment of Neurology, NeuroScienceLab, Medical Faculty, University Medicine Essen, 45147 Essen, Germany.
Andrea KutritzDepartment of Neurology, NeuroScienceLab, Medical Faculty, University Medicine Essen, 45147 Essen, Germany.
Tienush RassafDepartment of Cardiology and Vascular Medicine, CardioScienceLabs, University Medicine Essen, Medical Faculty, 45147 Essen, Germany.ORCID 0000-0001-8001-0265
Christoph KleinschnitzDepartment of Neurology, NeuroScienceLab, Medical Faculty, University Medicine Essen, 45147 Essen, Germany.
Ulrike B Hendgen-CottaDepartment of Cardiology and Vascular Medicine, CardioScienceLabs, University Medicine Essen, Medical Faculty, 45147 Essen, Germany.
Tim HagenackerDepartment of Neurology, NeuroScienceLab, Medical Faculty, University Medicine Essen, 45147 Essen, Germany.
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin and oxaliplatin are treatment options for a variety of cancer types. While highly efficient in killing cancer cells, both chemotherapeutics cause severe side effects, e.g., peripheral neuropathies. Using a cell viability assay, a mitochondrial stress assay, and live-cell imaging, the effects of cis- or oxaliplatin on the mitochondrial function, reactive oxygen species (ROS) production, and mitochondrial and cytosolic calcium concentration of transient receptor potential ankyrin 1 (TRPA1)- or vanilloid 1 (TRPV1)-positive dorsal root ganglion (DRG) neurons of adult Wistar rats were determined. Mitochondrial functions were impaired after exposure to cis- or oxaliplatin by mitochondrial respiratory chain complex I-III inhibition. The basal respiration, spare respiratory capacity, and the adenosine triphosphate (ATP)-linked respiration were decreased after exposure to 10 µM cis- or oxaliplatin. The ROS production showed an immediate increase, and after reaching the peak, ROS production dropped. Calcium imaging showed an increase in the cytosolic calcium concentration during exposure to 10 µM cis- or oxaliplatin in TRPA1- or TRPV1-positive DRG neurons while the mitochondrial calcium concentration continuously decreased. Our data demonstrate a significant effect of cis- and oxaliplatin on mitochondrial function as an early event of platinum-based drug exposure, suggesting mitochondria as a potential target for preventing chemotherapy-induced neuropathy.

Indexed as

AnimalsCalcium SignalingCells, CulturedFemaleGanglia, SpinalMaleMitochondriaMitochondrial ProteinsNeuronsOxaliplatinPeripheral Nervous System DiseasesRatsRats, WistarMitochondrial ProteinsOxaliplatinchemotherapycisplatindorsal root gangliamitochondrial stressneuropathic painneuropathyoxaliplatinperipheral nervous systemROSTRP channels

Identifiers

PMID33207782
PMCPMC7698191
OpenAlexW3099720051

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.