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SFB 1123:  Atherosclerosis: Mechanisms and Networks of Novel Therapeutic Targets

Subject Area Medicine
Biology
Term since 2014
Website Homepage
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 238187445
 
Vascular disease including coronary artery disease (CAD) and stroke is the leading cause of death and morbidity worldwide and imposes exorbitant socioeconomic costs. This dilemma could be alleviated by improving vascular prevention and therapy based on a refined mechanistic pervasion of atherosclerosis as the underlying pathology, prompting a more efficient and reliable identification of new candidates for potential translation to drug development. Beyond the emergence of PCSK9 inhibitors for efficient control of hyperlipidemia, the recent positive outcome of the CANTOS trial has lend convincing support to pursuing the concept that targeting inflammatory pathways has major impact in the pathogenesis and treatment of atherosclerosis. Thus, it remains the long-standing mission of the collaborative research center (CRC) 1123 to provide an in-depth mechanistic understanding of molecular networks in atherogenesis, atheroprogression and atherothrombosis and to improve the identification and validation of relevant therapeutic target candidates. The identification of relevant targets in such networks requires unbiased screening of different candidates, a thorough pathogenic basis and analysis of interactions in model systems. In the CRC1123, we persist on elaborating intricately linked molecular mechanisms of different target families - cytokines, signal proteins, nucleic acids and lipid mediators. To this end, we will implement state-of-the-art technology, namely genome editing and conditional mouse models for gene deletion or lineage tracking, proteomics, single cell RNA sequencing, spatial transcriptomics, and bioinformatics, and novel methods extending the limits of visualization, e.g. multiphoton, nanoscopic, optoacoustic or MS imaging. This will redefine the standards of target discovery and close methodological gaps to monitor cell trafficking, behavior, subcellular or molecular events in plaques or adventitia, as one key to the overall success of CRC1123 in a third period. Based on an excellent infrastructure and unique collaborative culture attracting outstanding junior scientists, CRC1123 will continue to decipher molecular and cellular determinants of atherosclerosis, giving rise to novel links between genetic, inflammatory and metabolic factors. By dissecting their interactions and combined effects, CRC1123 will provide valuable targets and therapeutic options with minimal side effects on immune responses and metabolic homeostasis.
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