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Polystyrene nanoplastics promote muscle cell senescence through microtubule hyper-stabilization-mediated mitophagy

Jie Cui1, Xianlin Yue2, Yajun Zhang1

  • 1School of Pharmaceutical Sciences, National Key Laboratory of Advanced Drug Delivery System, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.

Journal of Hazardous Materials
|July 15, 2025
PubMed

Insights

Polystyrene nanoplastics (NPs) damage muscle cells by disrupting microtubule networks, leading to organelle dysfunction and cellular senescence. Reactivating Sirt2 shows potential for mitigating NP-induced muscle damage.

Area of Science:

  • Cell Biology
  • Toxicology
  • Biochemistry

Background:

  • The impact of polystyrene nanoplastics (NPs) on skeletal muscle cells is not well understood.
  • Mechanisms underlying NP-induced cellular damage require further investigation.

Purpose of the Study:

  • To elucidate the effects of NPs on human skeletal muscle cells.
  • To identify the molecular mechanisms of NP-induced muscle cell damage and senescence.
  • To explore potential therapeutic targets for NP toxicity.

Main Methods:

  • Exposure of mice and cultured human muscle cells to polystyrene nanoplastics.
  • RNA sequencing to analyze gene expression changes.
  • Microtubule network analysis, including tubulin acetylation and dynamics.
  • Assessment of microtubule-organizing center (MTOC) function, mechanotransduction, and organelle trafficking.
  • Evaluation of mitochondrial damage, mitophagy, mtDNA leakage, and cGAS-Sting pathway activation.
  • Investigating the role of Sirt2 and HDAC6 in NP-induced microtubule alterations.

Main Results:

  • NPs were taken up by muscle cells, causing significant damage and altering cytoskeleton-related factors.
  • Internalized NPs disrupted the microtubule network, increasing tubulin acetylation and stabilization.
  • Impaired MTOC function, defective mechanotransduction (YAP deactivation), and compromised organelle trafficking (mitochondria, lysosomes) were observed.
  • Accumulation of damaged mitochondria, dysfunctional mitophagy, mtDNA leakage, and cGAS-Sting activation led to accelerated cellular senescence.
  • NP-induced hyper-acetylation was linked to Sirt2 and HDAC6 deactivation.
  • Sirt2 reactivation reduced NP-induced damage, senescence, and cytoplasmic NP levels.

Conclusions:

  • Polystyrene nanoplastics induce skeletal muscle cell senescence through microtubule network disruption.
  • Microtubule dynamics are a critical mediator of NP-induced cellular damage.
  • Deactivation of Sirt2 and HDAC6 drives NP-induced microtubule hyper-stabilization and subsequent toxicity.
  • Sirt2 reactivation presents a potential therapeutic strategy against nanoplastic-induced muscle damage.
Keywords:
CytoskeletonInnate immuneMechanical stressMicroplasticsMitochondrial damageNanoplastics

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