TY - JOUR
T1 - The heterogeneous cellular landscape of atherosclerosis
T2 - Implications for future research and therapies. A collaborative review from the EAS young fellows
AU - Bonacina, Fabrizia
AU - di Costanzo, Alessia
AU - Genkel, Vadim
AU - Kong, Xiang Yi
AU - Kroon, Jeffrey
AU - Stimjanin, Ena
AU - Tsiantoulas, Dimitrios
AU - Grootaert, Mandy O. J.
N1 - Funding Information: FB was supported by the Cariplo Foundation [ 2019–1560 ] and Roche Foundation for Research 2021 (Italy). XYK was supported by the South‐Eastern Norway Regional Health Authority (No. 2018064 ) and European Commission Research grant (PainFact, H2020-SC1-2019-2-RTD-848099 ). JK was supported by the Dutch Heart Foundation (Senior Scientist Dekker grant ( 03-004-2021-T045 )) and the European Research Council (ERC Starting grant ( 101076407 )). DT is supported by the European Research Council (ERC Starting grant ( 101041206 )), the Austrian Science Fund ( I4963 , P35233 ) and the European Research Area Network on Cardiovascular Diseases (ERA-CVD) ( I4647 ). MG is supported by ERA-CVD (ENRICH) and the Research Foundation Flanders (FWO - G0H7220 N ). Publisher Copyright: © 2023 Elsevier B.V.
PY - 2023/5/1
Y1 - 2023/5/1
N2 - 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.
AB - 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.
KW - Atherosclerosis therapy
KW - Cell activation
KW - Cell plasticity
KW - Cellular heterogeneity
KW - Intercellular communication
KW - Multi-omics
KW - Single cell RNA sequencing
UR - http://www.scopus.com/inward/record.url?scp=85151566580&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/j.atherosclerosis.2023.03.021
DO - https://doi.org/10.1016/j.atherosclerosis.2023.03.021
M3 - Review article
C2 - 37030081
SN - 0021-9150
VL - 372
SP - 48
EP - 56
JO - Atherosclerosis
JF - Atherosclerosis
ER -