ArticleJournal of cachexia, sarcopenia and muscle2026
Mitochondrial Transporter ABCB10 Protects Against Doxorubicin-Induced Respiratory Muscle Dysfunction Independent of Changes to Diaphragm Accumulation.
Article in Journal of cachexia, sarcopenia and muscle, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed.
- Antioxidant Upregulation Contributes to Improvements in Diaphragm Function Following Cervical Spinal Cord Injury and Hyperbaric Oxygen Therapy.Antioxidants (Basel, Switzerland) · 2026Article
- Acute mitochondrial dysfunction impairs neuromuscular transmission and contractility in mouse diaphragm: the protective potential of 25-hydroxycholesterol.Journal of physiology and biochemistry · 2026Article
- Mitochondrial Transporter ABCB10 Protects Against Doxorubicin-Induced Respiratory Muscle Dysfunction Independent of Changes to Diaphragm Accumulation.Journal of cachexia, sarcopenia and muscle · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundDoxorubicin (DOX) is a highly effective chemotherapeutic agent whose use can cause respiratory toxicity, increasing patient fatigue and negatively impacting quality of life and survival. These adverse effects occur due to diaphragm muscle mitochondrial accumulation of DOX, where it causes reactive oxygen species production and iron dysregulation. ABCB10 is a mitochondria-localized ATP-binding cassette transporter hypothesized to play a role in the maintenance of mitochondrial redox balance and iron homeostasis, and potentially the mitochondrial export of DOX. This study investigated potential therapeutic effects of ABCB10 to prevent DOX-induced respiratory muscle dysfunction.
methodsDOX respiratory muscle toxicity was modelled in rats using both single (20 mg/kg, once) and multicycle (5.7 mg/kg, 3 cycles) administration. The effects of overexpression and knockdown of ABCB10 on DOX-induced diaphragm dysfunction, mitochondrial DOX accumulation and markers of mitochondrial iron homeostasis were evaluated via administration of rAAV9-MHCK7-ABCB10 or an antisense oligonucleotide targeting ABCB10, respectively.
resultsABCB10 significantly improved diaphragm rate of fatigue (138.2 ± 11.66 s vs. 104.6 ± 8.79 s in DOX), specific force production (22.12 ± 0.70 N/cm
conclusionsThese results suggest that ABCB10 can preserve mitochondrial and diaphragm muscle function following DOX treatment by regulating iron redox-cycling and heme synthesis, independent of changes to DOX accumulation.
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Registered trials
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