Journal
CELLS
Volume 10, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/cells10030625
Keywords
autophagy; atherosclerosis; endothelial cells; vascular smooth-muscle cells; immune cells; microRNAs
Categories
Funding
- Deutsche Forschungsgemeinschaft (DFG) [403584255-TRR 267-A2, SFB1123-A1/A10]
- European Research Council (ERC) [692511]
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Atherosclerosis is a chronic inflammatory disease of the arterial vessel wall that leads to cardiovascular diseases, with cell-specific defective autophagy playing a crucial role in its pathogenesis. Research has shown the significance of autophagy in atherosclerosis development, presenting potential therapeutic implications for prevention and treatment of the disease.
Atherosclerosis is a chronic inflammatory disease of the arterial vessel wall and underlies the development of cardiovascular diseases, such as myocardial infarction and ischemic stroke. As such, atherosclerosis stands as the leading cause of death and disability worldwide and intensive scientific efforts are made to investigate its complex pathophysiology, which involves the deregulation of crucial intracellular pathways and intricate interactions between diverse cell types. A growing body of evidence, including in vitro and in vivo studies involving cell-specific deletion of autophagy-related genes (ATGs), has unveiled the mechanistic relevance of cell-specific (endothelial, smooth-muscle, and myeloid cells) defective autophagy in the processes of atherogenesis. In this review, we underscore the recent insights on autophagy's cell-type-dependent role in atherosclerosis development and progression, featuring the relevance of canonical catabolic functions and emerging noncanonical mechanisms, and highlighting the potential therapeutic implications for prevention and treatment of atherosclerosis and its complications.
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