Zinc oxide nanoparticles promote migrasomes formation.
Summary
ZnO nanoparticles (28 nm) enhance migrasome biogenesis linked to elevated PI(4,5)P2 and GTP-RhoA, and support mitocytosis to mitigate CCCP-induced mitochondrial damage. These findings suggest nanoparticle-driven modulation of intercellular communication and organelle quality control with implications for cosmetic safety and environmental health.
Key Findings
- 28 nm ZnO nanoparticles increase migrasome formation associated with elevated PI(4,5)P2 and GTP-RhoA.
- ZnO nanoparticles mitigate CCCP-induced mitochondrial damage via mitocytosis, preserving cellular integrity.
- ZnO-induced migrasomes contain mitochondria, lysosomes, lipid droplets, and ZnO nanoparticles.
Clinical Implications
Guides safety assessment of ZnO-containing sunscreens and topical products by highlighting potential effects on intercellular vesicle signaling and mitochondrial homeostasis.
Why It Matters
Reveals a mechanistic link between widely used cosmetic nanoparticle ZnO and migrasome biology/mitochondrial quality control, informing safer-by-design strategies and regulatory risk assessment.
Limitations
- In vitro study; lacks in vivo validation and dose–response relative to real-world exposure.
- Specific cell types and exposure conditions may limit generalizability to human tissues.
Future Directions
Define safe exposure windows in relevant skin models and in vivo; assess formulation-dependent effects and chronic exposure outcomes.
Study Information
- Study Type
- Basic/Mechanistic research
- Research Domain
- Pathophysiology
- Evidence Level
- V - In vitro mechanistic experiments without clinical participants
- Study Design
- OTHER