Evidence map›Paper›PMID 42386654›Full record

ArticleExperimental physiology2026

Impairments in mitochondrial dynamics and morphology in skeletal muscle of breast cancer patients after a single paclitaxel administration.

Joris Mallard, Elyse Hucteau, Laura Somme, Hervé Bischoff, Valérie Demais, Pauline Silvestrin, Anne-Laure Charles, Roland Schott, Xavier Pivot, Thomas J Hureau and 1 more

Abstract read
In one paragraph

Article in Experimental physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

Joris MallardExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.ORCID https://orcid.org/0009-0009-0890-3136
Elyse HucteauExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.ORCID https://orcid.org/0000-0002-9236-6514
Laura SommeExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.
Hervé BischoffExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.ORCID https://orcid.org/0000-0003-3382-9635
Valérie DemaisPlateforme Imagerie In Vitro, CNRS UPS-3156, NeuroPole, Strasbourg, France.
Pauline SilvestrinBiomedecine Research Center of Strasbourg (CRBS), UR 3072, 'Mitochondria, Oxidative Stress and Muscle Plasticity', University of Strasbourg, Strasbourg, France.
Anne-Laure CharlesBiomedecine Research Center of Strasbourg (CRBS), UR 3072, 'Mitochondria, Oxidative Stress and Muscle Plasticity', University of Strasbourg, Strasbourg, France.
Roland SchottExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.
Xavier PivotExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.
Thomas J HureauExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.ORCID https://orcid.org/0000-0002-6993-5723
Allan F PaganoExercise Physiology Laboratory, Institut Strauss, Strasbourg, France.

Funding

IdEx UnistraInstitut Strauss
6 · The paper itself

Abstract

Standard chemotherapy regimens for patients with breast cancer are based on epirubicin-cyclophosphamide (EC) and paclitaxel (TAX) administrations. While it has been shown that first EC administration impairs mitochondrial homeostasis, the isolated effects of TAX have not been studied without previous chemotherapy exposure. We conducted a prospective clinical study including five patients with breast cancer who underwent two vastus lateralis muscle biopsies before and 4 days after the first TAX administration, without any prior chemotherapy exposure. Mitochondrial respiratory capacity, reactive oxygen species production, mitochondrial dynamics and ultrastructure, and apoptosis were assessed using high-resolution respirometry, western blotting, transmission electron microscopy, and TUNEL assay, respectively. Post-TAX, the number of intermyofibrillar mitochondria decreased (-18%; P = 0.049), while the proportion of damaged mitochondria increased (+34%; P = 0.012). Mitochondrial area, perimeter and major/minor axis lengths increased (P < 0.05) while intermyofibrillar cristae area decreased (4.29% pre-TAX vs. 2.60% post-TAX; P = 0.044). Despite these morphological changes, oxidative phosphorylation capacity and respiratory control ratio remained unchanged, whereas complex I-linked substrate respiration decreased (-29%; P = 0.046). MFN2 (-43%; P = 0.040) and Fis1 (-46%; P = 0.046) protein levels decreased post-TAX while mitophagy markers were unchanged. Apoptosis was increased, as documented by increased Bax (+58%; P = 0.045) and TUNEL-positive nuclei (+395%; P = 0.041). In only 4 days, the first TAX administration induced severe skeletal muscle mitochondrial remodelling in patients with breast cancer, characterized by impaired mitochondrial dynamics that resulted in swollen and damaged organelles. These findings demonstrate that mitochondrial toxicity, classically documented at the end of treatment, occurs acutely and after only one chemotherapy administration.

Indexed as

Antineoplastic Agents, PhytogenicBreast NeoplasmsMitochondrial DynamicsMitochondria, MuscleMuscle, SkeletalPaclitaxelAdultApoptosisCyclophosphamideFemaleHumansMiddle AgedOxidative PhosphorylationProspective StudiesReactive Oxygen SpeciesAntineoplastic Agents, PhytogenicCyclophosphamidePaclitaxelReactive Oxygen Specieschemotherapymitochondrial dynamicsmitochondrial functionmuscle biopsiesmuscle homeostasisskeletal muscle deconditioning

Identifiers

PMID42386654
PMCPMC13394640

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Registered trials

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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.