Amorphous SiO2 nanoparticles promote cardiac dysfunction via the opening of the mitochondrial permeability transition pore in rat heart and human cardiomyocytes.

Omar LozanoChristian Silva-PlatasHéctor Chapoy-VillanuevaBaruc E PérezJarmon G LeesChrishan J A RamachandraFlavio F Contreras-TorresAnay Lázaro-AlfaroEstefanía Luna-FigueroaJudith Bernal-RamírezAldemar Gordillo-GaleanoAlfredo BenitezYuriana Oropeza-AlmazánElena C CastilloPoh Ling KohDerek J HausenloyShiang Y LimGerardo J García-Rivas

Published in: Particle and fibre toxicology (2020)

The aforementioned effects can be partially avoided reducing ROS or retarding the opening of the mPTP. These novel strategies which resulted in cardioprotection could be considered as potential therapies to decrease the side effects of nanoSiO2 exposure.

Keyphrases

oxidative stress
endothelial cells
dna damage
high glucose
heart failure
cell death
left ventricular
pluripotent stem cells
atrial fibrillation
room temperature
climate change
magnetic nanoparticles