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January 18, 2026Journal of Cachexia Sarcopenia and Muscle0 citationsOpen Access

ABCB10 Mitochondrial Transporter Prevents Doxorubicin-Induced Muscle Dysfunction

Mitochondrial Transporter ABCB10 Protects Against Doxorubicin‐Induced Respiratory Muscle Dysfunction Independent of Changes to Diaphragm Accumulation

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Why the study?

Does ABCB10 overexpression prevent doxorubicin-induced respiratory muscle dysfunction in a rat model?

Population

Female Sprague-Dawley rats modeling doxorubicin-induced respiratory muscle toxicity.

Comparison

Overexpression of ABCB10 via rAAV9-MHCK7-ABCB10… vs Saline vector or saline antisense…

Design

Preclinical

Follow-up

2 days following single doxorubicin dose or 2 days…

Key result

ABCB10 improved diaphragm fatigue (138.2 s vs. 104.6 s), specific force (22.12 N/cm² vs. 18.31 N/cm²), and fibre area in rats treated with doxorubicin, independent of drug accumulation.

Authors

ASAshley J. SmuderVDVivian DoerrCMCesar E. Jacintho Moritz

Discussion

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Overview

Should not change clinical practice; hypothesis-generating for ABCB10 in anthracycline myotoxicity.

Key Points

  • Investigate the protective role of ABCB10 against doxorubicin-induced respiratory muscle dysfunction and its mechanisms.
  • Modeling doxorubicin respiratory muscle toxicity in rats through single and multicycle administration.
  • Evaluating effects of overexpression and knockdown of ABCB10 on diaphragm dysfunction and mitochondrial accumulation.
  • Analyzing mitochondrial iron homeostasis and related gene expressions post-treatment.
  • ABCB10 improved diaphragm fatigue rate and specific force production in doxorubicin-treated rats.
  • Diaphragm fiber area increased with ABCB10 intervention despite unchanged doxorubicin accumulation.
  • Reduced mitochondrial iron levels and altered gene expressions linked to iron and heme synthesis were observed.

Structured PICO

Does ABCB10 overexpression prevent doxorubicin-induced respiratory muscle dysfunction in a rat model?

P
Population
Female Sprague-Dawley rats (n=112 total; Experiments 1 and 2 n=10/group, Experiment 3 n=8/group) modeling doxorubicin-induced respiratory muscle toxicity.
I
Intervention
Overexpression of ABCB10 via rAAV9-MHCK7-ABCB10 (10^11 vg IV) or knockdown via antisense oligonucleotide targeting ABCB10 (60 mg/kg IP for 5 days), combined with doxorubicin (single dose 20 mg/kg, or multicycle 5.7 mg/kg for 3 cycles).
C
Comparator
Saline vector or saline antisense oligonucleotide control, and saline injection in place of doxorubicin.
O
Outcome
Diaphragm rate of fatigue, specific force production, and muscle fiber cross-sectional area.surrogate

ABCB10 overexpression protects against doxorubicin-induced diaphragm muscle weakness by regulating mitochondrial iron and heme synthesis, independent of doxorubicin accumulation.

Cite This Study

Smuder et al. (2026) studied this question. ABCB10 improved diaphragm fatigue (138.2 s vs. 104.6 s), specific force (22.12 N/cm² vs. 18.31 N/cm²), and fibre area in rats treated with doxorubicin, independent of drug accumulation.

synapsesocial.com/papers/696c77f1eb60fb80d1396390https://doi.org/10.1002/jcsm.70171
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Effects of Mitochondrial ABCB7 Transporter Upregulation on Acute Doxorubicin Cardiorespiratory Muscle Injury2026
  2. 2Targeting mitochondrial dysfunction with the exercise-derived metabolite beta-aminoisobutyric acid protects against doxorubicin-induced cardiomyopathy2026
  3. 3Effect of age on the development of acute Doxorubicin-induced respiratory muscle dysfunction2026
  4. 4Effects of exercise and doxorubicin on acute diaphragm neuromuscular transmission failure2024 · 2 citations
  5. 5Doxorubicin-induced oxidative stress differentially regulates proteolytic signaling in cardiac and skeletal muscle2019 · 77 citations