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Related Experiment Video

Updated: Jan 17, 2026

Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues

Preclinical Drug Testing in Scalable 3D Engineered Muscle Tissues

Published on: April 7, 2023

TNF-α-induced contractile dysfunction in three-dimensional engineered muscle.

Yukinori Tamura¹, Junpei Ishizaka¹, Sho Yokoyama²

¹Division of Physiology and Biochemistry, Faculty of Nutrition, Kobe Gakuin University, 518 Arise, Ikawadani-cho, Nishi-ku, Kobe 651-2180, Japan.

Journal of Bioscience and Bioengineering

|January 14, 2026

Summary

Tumor necrosis factor-alpha (TNF-α) significantly weakens engineered muscle by damaging its structure and contractile function. This cytokine impairs extracellular matrix, sarcomeres, and calcium signaling, offering insights into sarcopenia mechanisms.

Keywords:

Calcium signaling Excitation–contraction coupling Extracellular matrix Muscle weakness Three-dimensional engineered muscle Tumor necrosis factor-α

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Published on: March 19, 2013

Area of Science:

Muscle physiology
Biomedical engineering
Inflammation research

Background:

Skeletal muscle weakness is a hallmark of conditions like sarcopenia and cachexia.
Tumor necrosis factor-alpha (TNF-α) is implicated in muscle weakness, but its direct mechanisms are not fully understood.
Three-dimensional engineered muscle (3D-EM) offers a physiologically relevant model for studying muscle function.

Purpose of the Study:

To investigate the direct impact of TNF-α on the contractile force of 3D-EM.
To elucidate the molecular and structural mechanisms by which TNF-α induces muscle weakness.

Main Methods:

3D-EM constructs were created using C2C12 myoblasts and type I collagen.
Constructs were treated with TNF-α, and contractile force was measured via electrical pulse stimulation.
Immunohistochemistry and RNA sequencing (RNA-seq) were used to analyze structural and transcriptomic changes.

Main Results:

TNF-α treatment led to a 60% reduction in contractile force after 48 hours and a 90% reduction after 72 hours.
Immunohistochemistry revealed myotube atrophy and loss of fast-twitch fibers.
RNA-seq analysis indicated suppressed pathways related to extracellular matrix, sarcomere organization, and calcium signaling.

Conclusions:

TNF-α impairs force generation in 3D-EM by disrupting extracellular matrix integrity, sarcomeric structure, and calcium-dependent contraction.
Fast-twitch muscle fibers are preferentially affected by TNF-α.
3D-EM serves as a valuable model for understanding cytokine-induced muscle weakness and sarcopenia.