ArticleScientific reports2024
Molecular and clinical effects of aromatase inhibitor therapy on skeletal muscle function in early-stage breast cancer.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 2 citations in OpenAlex.
- Creatinine-Cystatin C Discrepancy and Renal Transporter Polymorphisms in Japanese Patients with Breast Cancer Receiving Abemaciclib.Clinical pharmacology and therapeutics · 2026Article
- Resistance Exercise Training Selectively Modulates Tumor Suppressor and Muscle-Regulatory MicroRNAs in Breast Cancer Survivors and Healthy Postmenopausal Women: An Exploratory Study.International journal of molecular sciences · 2026Article
- Single-fiber morphometry and spatial transcriptomics reveal selective oxidative muscle fiber atrophy in non-metastatic breast cancer.medRxiv : the preprint server for health sciences · 2026Article
- Aerobic exercise modalities on gut microbiome and skeletal muscle quality in ovariectomized mice.Frontiers in cellular and infection microbiology · 2025Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
We evaluated biochemical changes in skeletal muscle of women with breast cancer initiating aromatase inhibitors (AI), including oxidation of ryanodine receptor RyR1 and loss of stabilizing protein calstabin1, and detailed measures of muscle function. Fifteen postmenopausal women with stage I-III breast cancer planning to initiate AI enrolled. Quadriceps muscle biopsy, dual-energy x-ray absorptiometry, isokinetic dynamometry, Short Physical Performance Battery, grip strength, 6-min walk, patient-reported outcomes, and serologic measures of bone turnover were assessed before and after 6 months of AI. Post-AI exposure, oxidation of RyR1 significantly increased (0.23 ± 0.37 vs. 0.88 ± 0.80, p < 0.001) and RyR1-bound calstabin1 significantly decreased (1.69 ± 1.53 vs. 0.74 ± 0.85, p < 0.001), consistent with dysfunctional calcium channels in skeletal muscle. Grip strength significantly decreased at 6 months. No significant differences were seen in isokinetic dynamometry measures of muscle contractility, fatigue resistance, or muscle recovery post-AI exposure. However, there was significant correlation between oxidation of RyR1 with muscle power (r = 0.60, p = 0.02) and muscle fatigue (r = 0.57, p = 0.03). Estrogen deprivation therapy for breast cancer resulted in maladaptive changes in skeletal muscle, consistent with the biochemical signature of dysfunctional RyR1 calcium channels. Future studies will evaluate longer trajectories of muscle function change and include other high bone turnover states, such as bone metastases.
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Registered trials
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