Single cell technologies, lineage tracing mouse models and advanced imaging techniques
unequivocally improved the resolution of the cellular landscape of atherosclerosis.
Although the discovery of the heterogeneous nature of the cellular plaque architecture
has undoubtedly improved our understanding of the specific cellular states in atherosclerosis
progression, it also adds more complexity to current and future research and will
change how we approach future drug development. In this review, we will discuss how
the revolution of new single cell technologies allowed us to map the cellular networks
in the plaque, but we will also address current (technological) limitations that confine
us to identify the cellular drivers of the disease and to pinpoint a specific cell
state, cell subset or cell surface antigen as new candidate drug target for atherosclerosis.
