Cited by 48Muscle Physiology and DisordersInflammasome and immune disordersMitochondrial Function and Pathology

Mitochondrial dysfunction/NLRP3 inflammasome axis contributes to angiotensin II-induced skeletal muscle wasting via PPAR-γ

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Liu, Yuqing, Bi, Xiao, Zhang, Yumei, Wang, Yingdeng, Ding, Wei·2020·Laboratory Investigation

Abstract

Angiotensin II (Ang II) levels are elevated in patients with chronic kidney disease or heart failure, and directly causes skeletal muscle wasting in rodents, but the molecular mechanisms of Ang II-induced skeletal muscle wasting and its potential as a therapeutic target are unknown. We investigated the NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated muscle atrophy response to Ang II in C2C12 myotubes and Nlrp3 knockout mice. We also assessed the mitochondrial dysfunction (MtD)/NLRP3 inflammasome axis in Ang II-induced C2C12 myotubes. Finally, we examined whether a peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist could attenuate skeletal muscle wasting by targeting the MtD/NLRP3 inflammasome axis in vitro and in vivo. We demonstrated that Ang II increased NLRP3 inflammasome activation in cultured C2C12 myotubes dose dependently. Nlrp3 knockdown or Nlrp3-/- mice were protected from the imbalance of protein synthesis and degradation. Exposure of C2C12 to Ang II increased mitochondrial ROS (mtROS) generation, accompanied by MtD. Remarkably, the mitochondrial-targeted antioxidant not only decreased mtROS and MtD, it also significantly inhibited NLRP3 inflammasome activation and restored skeletal muscle atrophy. Finally, the PPAR-γ agonist protected against Ang II-induced muscle wasting by preventing MtD, oxidative stress, and NLRP3 inflammasome activation in vitro and in vivo. This work suggests a potential role of MtD/NLRP3 inflammasome pathway in the pathogenesis of Ang II-induced skeletal muscle wasting, and targeting the PPAR-γ/MtD/NLRP3 inflammasome axis may provide a therapeutic approach for muscle wasting.

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Crossref · 10.1038/s41374-019-0355-1

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  • Alterations in mPTP function contribute to the aging-related loss of muscle mass and function.

    “Alterations in mPTP function are undoubtedly contributing to the aging-related loss of muscle mass and function, since mPTP opening can trigger several atrophy-regulating pathways.”

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Authors
Liu, Y., Bi, X., Zhang, Y., Wang, Y., & Ding, W.
Affiliations
Shanghai Jiao Tong University (CN)
Corresponding author
Ding, Wei
Venue
Laboratory Investigation
Publisher
Elsevier BV
Published
2020-05
Volume
100
Issue
5
Pages
712-726
ISSN
0023-6837 (ISSN-L)
OpenAlex
W2996604018
Cited by
48
References
36
Citations by year
2026: 7 · 2025: 7 · 2024: 5 · 2023: 6 · 2022: 8 · 2021: 13 · 2020: 2
FWCI
1.91
Type
journal article
Language
en
Open access
Locations
  • Laboratory Investigation (publishedVersion)
  • SSRN Electronic Journal (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
angiotensin II, skeletal muscle atrophy, NLRP3 inflammasome, mitochondrial dysfunction, PPARγ agonists, mitochondrial reactive oxygen species, oxidative stress, muscle atrophy, protein synthesis and degradation, chronic kidney disease, heart failure, NLRP3 knockout mice, C2C12 myotubes
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, Angiotensin II, Animals, Cell Line, Mice, Inbred C57BL, Mitochondria, Muscular Atrophy, Mice, Knockout, Muscle, Skeletal, PPAR gamma, Mice

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