Role of autophagy in atherosclerosis: foe or friend?
Mehdi HassanpourReza RahbarghaziMohammad NouriNasser AghamohammadzadehNasser SafaeiMahdi AhmadiPublished in: Journal of inflammation (London, England) (2019)
Athrosclerosis is conceived as a chronic inflammatory status affecting cells from vascular walls. Different mechanisms and pathological features are evident at the onset of atherosclerotic changes via the engaging different cells from the vascular wall and circulatory cells. Attempts are currently focused on the detection of cell compensatory mechanisms against atherosclerotic changes to restore cell function and/or postpone severe vasculitis. Autophagy is an intracellular self-digesting process commonly protrudes exhausted organelles and injured cytoplasmic constituents via double-lipid bilayer membrane vesicles out the target cells. Recent investigations point to the critical and defensive role of autophagy in the vascular cells behavioral function such as endothelial cells and smooth muscle cells against different insults. Autophagy response and related effectors could be modulated in the favor to restore cell function and reduce pro-inflammatory status under pathological conditions. In this review, the recent findings were collected regarding the role of autophagy during atherosclerotic changes. We aimed to answer the question of how autophagy stimulation and/or inhibition could provide a promising effect on developing a sophisticated treatment for AS.
Keyphrases
- induced apoptosis
- endoplasmic reticulum stress
- cell death
- cell cycle arrest
- oxidative stress
- signaling pathway
- endothelial cells
- pi k akt
- cardiovascular disease
- type diabetes
- stem cells
- extracorporeal membrane oxygenation
- mesenchymal stem cells
- early onset
- cell proliferation
- high glucose
- reactive oxygen species
- combination therapy
- sensitive detection
- real time pcr