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Defective Autophagy in Atherosclerosis: To Die or to Senesce?
Mandy O J Grootaert1, Lynn Roth1, Dorien M Schrijvers2
1Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.
Oxidative Medicine and Cellular Longevity
|April 24, 2018
Summary
Autophagy, a cellular cleanup process, becomes faulty in atherosclerosis. This defective autophagy impacts different cells in blood vessels, affecting disease progression and treatment strategies.
Area of Science:
- Cellular Biology
- Molecular Medicine
- Cardiovascular Research
Background:
- Autophagy is a vital cellular degradation process for maintaining homeostasis.
- Dysfunctional autophagy is linked to various diseases, including atherosclerosis.
- Atherosclerotic plaques exhibit impaired autophagy despite pro-autophagy signals.
Purpose of the Study:
- To review recent findings on defective autophagy in atherosclerosis.
- To explore the role of autophagy and mitophagy in key vascular cells.
- To discuss cell-specific consequences of autophagy deficiency.
Main Methods:
- Literature review of current research on autophagy in atherosclerosis.
- Focus on autophagy's role in macrophages, VSMCs, and ECs.
- Analysis of cell-type-specific responses to autophagy defects.
Main Results:
- Defective autophagy promotes macrophage apoptosis.
- Defective autophagy accelerates VSMC senescence.
- Defective autophagy induces both apoptosis and senescence in ECs.
Conclusions:
- Autophagy plays a cell-dependent role in atherosclerosis.
- Understanding these differences is crucial for developing targeted therapies.
- Autophagy dysfunction contributes to atherosclerotic plaque development.
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