Atg5 deficit exaggerates the lysosome formation and cathepsin B activation in mice brain after lipid nanoparticles injection

The aggregation of lipid nanoparticles in brain induces an excessive activation of the autophagy-lysosome pathway via an Atg5-dependent manner, which might represent a compromise cellular mechanism that contributes to the neuroinflammatory response. Furthermore, the Atg5 deficit exaggerates the lipid nanoparticles-induced neurovascular response through promoting lysosome formation and cathepsin B activation in mice brain.188