Marco E. Zamora

This paper identifies that lipid nanoparticle-induced inflammation arises from endosomal membrane damage and proposes strategies to mitigate it through galectin inhibition or ESCRT-recruiting lipids.

The paper identifies a critical threshold in complement activation based on surface density, showing percolation-type behavior in immune responses to materials.

The paper shows that lung marginated neutrophils effectively uptake endothelial-targeted nanoparticles, suggesting they are part of the reticuloendothelial system.

This paper combines affinity moiety targeting and physicochemical tropism in lipid nanoparticles to enhance organ targeting, showing improved specificity and uptake in lungs and brain.