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May 13, 2026Cellular Physiology and BiochemistryOpen Access

Effects of Urolithin A on Mitochondrial Homeostasis Disruption by LPS in C2C12 Myotubes

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This study investigates the effects of urolithin A on mitochondrial homeostasis disruption induced by LPS in C2C12 myotubes.
Incubation of C2C12 myotubes with LPS and/or urolithin A.
Assessment of protein expression related to TLR4 signaling and mitochondrial dynamics by Western blot.
Evaluation of mitochondrial morphology using electron microscopy.
LPS induced inflammation activating TLR4 signaling pathways leading to altered mitochondrial morphology.
LPS increased phosphorylation of the mitochondrial fission marker DRP1.
Urolithin A prevented or attenuated reductions in mitochondrial area and circularity caused by LPS.

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Implication

Experimental findings reveal that urolithin A reduces inflammation and improves mitochondrial homeostasis in C2C12 myotubes, implying therapeutic strategy for mitochondrial dysfunction.

Cite This Study

Tapia‐Curimil et al. (2026) studied this question.

synapsesocial.com/papers/6a03cbfc1c527af8f1ecfdaf https://doi.org/10.33594/000000869

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Implication

Experimental findings reveal that urolithin A reduces inflammation and improves mitochondrial homeostasis in C2C12 myotubes, implying therapeutic strategy for mitochondrial dysfunction.

Effects of Urolithin A on Mitochondrial Homeostasis Disruption by LPS in C2C12 Myotubes

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Discussion

Implication

Cite This Study

Effects of Urolithin A on Mitochondrial Homeostasis Disruption by LPS in C2C12 Myotubes

Key Points

Discussion

Implication

Cite This Study

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