Sialidase Neu3 Induced Sialic Acid Disorder and Promoted Vascular Endothelial Injury Through Transcription Factor SP3

mice as well as atherosclerotic patient tissues. Mechanically, we found that the transcription factor specificity protein 3 (SP3) was activated in HUVECs, responsible for Neu5Ac metabolism disorder. While RNA interference of SP3 could decrease NEU3 mRNA level and reduce endothelial inflammatory injury, indicating that SP3 might be the upstream regulatory factor of NEU3. Together, these findings identified the key role of NEU3 in regulating Neu5Ac metabolism associated with endothelial function, as well as its potential regulation mechanism. Targeting SP3/NEU3 seems to be a potential therapeutic strategy for such diseases with Neu5Ac accumulation like atherosclerosis (AS).