Evidence map›Paper›PMID 34182057›Full record

ReviewNeuroscience letters2021

Mini-Review: Mitochondrial dysfunction and chemotherapy-induced neuropathic pain.

Timothy M Doyle, Daniela Salvemini

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

76 citing papers in PubMed, 99 citations in OpenAlex.

  1. Efficacy and safety of Lignosus rhinocerus (Cooke) Ryvarden TM02BMC complementary medicine and therapies · 2025
    Trial
  2. Review
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  4. Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Article
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  7. Betanin fromBiomedicines · 2026
    Article
  8. Article
  9. Review
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  16. Article
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  19. Article
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16 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

2 authors at 1 institution in 1 country.

Timothy M DoyleDepartment of Pharmacology and Physiology, Saint Louis University School of Medicine, 1402 S. Grand Blvd, St. Louis, MO 63104, USA; Henry and Amelia Nasrallah Center for Neuroscience, Saint Louis University School of Medicine, 1402 S. Grand Blvd, St. Louis, MO 63104, USA.
Daniela SalveminiDepartment of Pharmacology and Physiology, Saint Louis University School of Medicine, 1402 S. Grand Blvd, St. Louis, MO 63104, USA; Henry and Amelia Nasrallah Center for Neuroscience, Saint Louis University School of Medicine, 1402 S. Grand Blvd, St. Louis, MO 63104, USA. Electronic address: daniela.salvemini@health.slu.edu.
Saint Louis University · US

Funding

A3AR agonists as a novel approach to mitigate chemotherapy induced neurotoxicityR01CA230512 · NCI · SAINT LOUIS UNIVERSITY · PI SALVEMINI, DANIELA · 2018 to 2022
$2.8M
Role of peroxynitrite in morphine hyperalgesia and toleranceR01DA024074 · NIDA · SAINT LOUIS UNIVERSITY · PI SALVEMINI, DANIELA · 2008 to 2012
$1.7M
A3AR agonists to prevent chemotherapy-induced painful peripheral neuropathyR01CA169519 · NCI · SAINT LOUIS UNIVERSITY · PI SALVEMINI, DANIELA · 2013 to 2017
$1.5M
NCI NIH HHS R01 CA169519NCI NIH HHS R01 CA230512NIDA NIH HHS R01 DA024074
6 · The paper itself

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a somatosensory axonopathy in cancer patients receiving any of a variety of widely-use antitumor agents. CIPN can lead to long-lasting neuropathic pain that limits the dose or length of otherwise life-saving cancer therapy. Accumulating evidence over the last two decades indicates that many chemotherapeutic agents cause mitochondrial injury in the peripheral sensory nerves by disrupting mitochondrial structure and bioenergetics, increasing nitro-oxidative stress and altering mitochondrial transport, fission, fusion and mitophagy. The accumulation of abnormal and dysfunctional mitochondria in sensory neurons are linked to axonal growth defects resulting in the loss of intraepidermal nerve fibers in the hands and feet, increased spontaneous discharge and the sensitization of peripheral sensory neurons that provoke and promote changes in the central nervous system that establish a chronic neuropathic pain state. This has led to the propose mitotoxicity theory of CIPN. Strategies that improve mitochondrial function have shown success in preventing and reversing CIPN in pre-clinical animal models and have begun to show some progress toward translation to the clinic. In this review, we will review the evidence for, the causes and effects of and current strategies to target mitochondrial dysfunction in CIPN.

Indexed as

AnimalsAntineoplastic AgentsAxonsDisease Models, AnimalHumansMitochondriaNeoplasmsNeuralgiaSensory Receptor CellsAntineoplastic AgentsBioenergeticsChemotherapy-induced neuropathyMitochondrial dysfunctionMitochondrial transportNeuropathic painNitro-oxidative stress

Identifiers

PMID34182057
PMCPMC9260825
OpenAlexW3174746712

What OpenQuestion holds

Textmetadata
LicenceTDM
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.