Novel PMVs/ZIP4/Zinc/Prelamin A Axis Promotes Nuclear Dysmorphism and Vascular Aging in Humans and Rodents Post-Injury: Effective Treatment With Platelet Membrane-Coated ZIF-8 Nanoparticles - PubMed
2 days ago
- #zinc deficiency
- #vascular aging
- #nuclear dysmorphism
- Interventional therapy and surgery can cause vascular injury, leading to nuclear dysmorphism and vascular aging.
- Platelet-derived microvesicles (PMVs) adhere to injured blood vessels, reducing intracellular Zn2+ levels and impairing prelamin A processing.
- Zinc transporter ZIP4 deficiency contributes to decreased zinc levels, exacerbating nuclear dysmorphism and vascular aging.
- Zmpste24-deficient mice show increased prelamin A accumulation, nuclear dysmorphism, and vascular aging.
- Demethylation of genes in Lamina-associated domains (LADs) plays a role in nuclear dysmorphism and cell senescence.
- Zinc supplementation, especially with platelet membrane-coated Zn-MOF nanoparticles, effectively alleviates these aging effects.