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Inflammation, lipids, and free radicals: lessons learned from the atherogenic process
1Department of Pathobiology, University of Washington, Seattle 98195, USA.
Seminars in Reproductive Endocrinology
|April 2, 1999
Summary
Oxidative stress in atherosclerotic lesions drives gene expression, cell proliferation, and cell death. This process contributes to lesion initiation, progression, and instability, impacting cardiovascular health.
Area of Science:
- Cardiovascular Biology
- Cellular Stress Response
- Atherosclerosis Research
Background:
- Atherosclerotic lesions involve cellular oxidative stress.
- Oxidative stress impacts gene expression, proliferation, and cell death.
- Reduced glutathione depletion is a key factor in cellular oxidative stress.
Purpose of the Study:
- To review how oxidative stress in atherosclerotic lesions influences cellular processes.
- To examine the contribution of oxidative stress to lesion development and destabilization.
- To explore the mechanisms of oxidative stress in lesion-resident cells.
Main Methods:
- Review of in vitro and in vivo evidence.
- Analysis of cellular responses to modified lipoproteins and oxidized lipids.
- Examination of redox-sensitive signaling pathways and transcription factors.
Main Results:
- Oxidative stress, driven by factors like oxidized lipids and reactive oxygen species, affects endothelial cells, macrophages, and smooth muscle cells.
- Sublethal oxidative stress activates signaling pathways (e.g., NFB, AP-1), promoting inflammation and proliferation.
- Severe oxidative stress induces apoptosis and necrosis, contributing to the necrotic core of advanced lesions.
Conclusions:
- Oxidative stress is a critical mediator in the pathogenesis of atherosclerosis.
- Cellular responses to oxidative stress, including proliferation and death, dictate lesion progression and stability.
- Understanding these mechanisms is crucial for developing therapeutic strategies against atherosclerotic disease.