Zinc regulates Nox1 expression through a NF-¿B and mitochondrial ROS dependent mechanism to induce senescence of vascular smooth muscle cells

Salazar G, etc|Free Radical Biology and Medicine|Florida State University

Increased Nox1 expression by zinc mediates senescence of VSMCs by telomere-dependent and -independent mechanisms.

  • Overexpression of ZnT3 or ZnT10 reduces Nox1 expression, while ZnT3 gene deficiency increases Nox1.

  • Zinc accumulates in mitochondria increasing mitochondrial ROS.

  • Zinc stimulates NF-¿B activation in VSMCs.

  • Inhibition of NF-¿B activation and reduction of mitochondrial ROS reduces Nox1 expression and prevents zinc-induced senescence.

    • Salazar G & etc. (2017). Zinc regulates Nox1 expression through a NF-¿B and mitochondrial ROS dependent mechanism to induce senescence of vascular smooth muscle cells. Free Radical Biology and Medicine, doi: 10.1016/j.freeradbiomed.2017.03.032