| Literature DB >> 33799835 |
James M Henderson1,2, Christian Weber1,2,3,4, Donato Santovito1,2,5.
Abstract
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.Entities:
Keywords: atherosclerosis; autophagy; endothelial cells; immune cells; microRNAs; vascular smooth-muscle cells
Year: 2021 PMID: 33799835 PMCID: PMC7998923 DOI: 10.3390/cells10030625
Source DB: PubMed Journal: Cells ISSN: 2073-4409 Impact factor: 6.600