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Assessing Functional Metrics of Skeletal Muscle Health in Human Skeletal Muscle Microtissues
Published on: February 18, 2021
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Modeling statin myopathy in a human skeletal muscle microphysiological system
Anandita Ananthakumar1, Yiling Liu2, Cristina E Fernandez1
1Department of Biomedical Engineering, Duke University, Durham, NC, United States of America.
Plos One
|November 25, 2020
Summary
Statins can cause muscle problems (SAMS). This study found statins reduced muscle fiber force in engineered human muscle cells, but did not show differences between cells from patients with or without SAMS.
Area of Science:
- Biomedical Engineering
- Skeletal Muscle Physiology
- Pharmacology
Background:
- Statins are crucial for cardiovascular disease prevention but can cause statin-associated musculoskeletal symptoms (SAMS) in up to 10% of users.
- SAMS necessitate treatment interruption, potentially increasing cardiovascular risk.
- Understanding the cellular mechanisms of SAMS is vital for patient management.
Purpose of the Study:
- To investigate whether engineered human skeletal myobundles from individuals with or without SAMS exhibit differential responses to statin exposure ex vivo.
- To identify potential biomarkers or mechanisms underlying statin-induced myotoxicity.
Main Methods:
- Engineered human skeletal myobundles were derived from myoblasts of individuals with (n=10) or without (n=14) SAMS.
- Myobundles were cultured and exposed to varying concentrations of statins (0 and 5μM) for 5 days.
- Tetanus forces were measured, and immunofluorescence was used to quantify muscle fiber integrity.
Main Results:
- Statin exposure significantly decreased muscle force and increased data variability (P<0.001).
- No significant differences in force reduction were observed between myobundles from SAMS-positive and SAMS-negative donors.
- Statin exposure correlated with reduced striated muscle fibers and increased fragmented fibers, but these changes did not differ between donor groups.
Conclusions:
- Statin exposure induces myotoxicity in engineered human skeletal myobundles, disrupting muscle organization and reducing force.
- This study did not identify inherent ex vivo differences in statin myotoxicity between individuals with or without SAMS.
- The findings suggest that inherent susceptibility or persistent effects of statin myopathy may not be evident in this patient-derived myobundle model.
