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The NLRP3 Mediates Masticatory Muscle Atrophy by Pyroptosis and Mitophagy.

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Názov: The NLRP3 Mediates Masticatory Muscle Atrophy by Pyroptosis and Mitophagy.
Autori: Li, Q., Gao, A., Wu, C., Song, X., Liu, W., Cheng, Y., Li, T., Zhang, K., Chen, Y., Liu, X., Hong, Y., Wu, T.
Zdroj: Journal of Dental Research; Dec2025, Vol. 104 Issue 13, p1556-1566, 11p
Predmety: NLRP3 protein, PYROPTOSIS, MASTICATORY muscles, MITOCHONDRIA, ORTHODONTICS, MITOCHONDRIAL pathology, MUSCULAR atrophy, MUSCLE diseases
Abstrakt: Masticatory muscle atrophy is relatively common and affects occlusal function, facial appearance, and even quality of life. The molecular mechanisms underlying changes in the masticatory muscles remain largely unknown. The Nod-like receptor protein 3 (NLRP3) inflammasome has been extensively reported to be associated with various myopathies; however, little is known about its role in masticatory muscle atrophy. Here, we investigated the function and underlying mechanisms of NLRP3 inflammasome activation in muscle atrophy models both in vitro and in vivo. First, significant atrophy of the masticatory muscles was observed after excessive orthodontic traction in rats, with NLRP3 inflammasome activation leading to increased myocyte pyroptosis. Further observations in the atrophied masticatory muscles revealed a significant reduction in mitochondrial number and overactivation of mitophagy. Conversely, inhibiting NLRP3 suppressed the expression of pyroptosis-related proteins and alleviated muscle atrophy. Moreover, blocking the activation of the NLRP3 inflammasome considerably alleviated mitochondrial dysfunction in the atrophied masticatory muscles and reduced excessive mitophagy, thereby maintaining intracellular homeostasis and preserving muscle mass. In addition, the results of the in vitro experiments confirmed that knocking down NLRP3 significantly alleviated NLRP3 agonist-induced pyroptosis and atrophy in the myotubes, improved mitochondrial damage, maintained mitochondrial membrane potential (Δψm), and decreased reactive oxygen species production. In summary, this study demonstrates that the NLRP3 inflammasome induces pyroptosis, mitochondrial dysfunction, and mitophagy, thereby becoming an important regulatory factor for masticatory muscle atrophy. Our research provides new insights into the mechanism of masticatory muscle atrophy. [ABSTRACT FROM AUTHOR]
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Databáza: Complementary Index
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Abstrakt:Masticatory muscle atrophy is relatively common and affects occlusal function, facial appearance, and even quality of life. The molecular mechanisms underlying changes in the masticatory muscles remain largely unknown. The Nod-like receptor protein 3 (NLRP3) inflammasome has been extensively reported to be associated with various myopathies; however, little is known about its role in masticatory muscle atrophy. Here, we investigated the function and underlying mechanisms of NLRP3 inflammasome activation in muscle atrophy models both in vitro and in vivo. First, significant atrophy of the masticatory muscles was observed after excessive orthodontic traction in rats, with NLRP3 inflammasome activation leading to increased myocyte pyroptosis. Further observations in the atrophied masticatory muscles revealed a significant reduction in mitochondrial number and overactivation of mitophagy. Conversely, inhibiting NLRP3 suppressed the expression of pyroptosis-related proteins and alleviated muscle atrophy. Moreover, blocking the activation of the NLRP3 inflammasome considerably alleviated mitochondrial dysfunction in the atrophied masticatory muscles and reduced excessive mitophagy, thereby maintaining intracellular homeostasis and preserving muscle mass. In addition, the results of the in vitro experiments confirmed that knocking down NLRP3 significantly alleviated NLRP3 agonist-induced pyroptosis and atrophy in the myotubes, improved mitochondrial damage, maintained mitochondrial membrane potential (Δψm), and decreased reactive oxygen species production. In summary, this study demonstrates that the NLRP3 inflammasome induces pyroptosis, mitochondrial dysfunction, and mitophagy, thereby becoming an important regulatory factor for masticatory muscle atrophy. Our research provides new insights into the mechanism of masticatory muscle atrophy. [ABSTRACT FROM AUTHOR]
ISSN:00220345
DOI:10.1177/00220345251344295