LDL oxidation, or oxidized LDL (oxLDL), represents a variety of modifications of both lipid and apolipoprotein B (apoB) components by lipid peroxidation. This process is significant because it contributes to the development of atherosclerosis.
Understanding LDL Oxidation
LDL, or low-density lipoprotein, is often referred to as "bad" cholesterol. Its primary function is to transport cholesterol throughout the body. When LDL particles become oxidized, they undergo significant changes that promote inflammation and the formation of plaque in arteries.
Key Aspects of LDL Oxidation:
- Lipid Peroxidation: The lipids within the LDL particle undergo oxidation.
- ApoB Modification: The apolipoprotein B (apoB), a protein component of LDL, is also modified.
- Atherosclerosis Promotion: Oxidized LDL (oxLDL) promotes atherosclerosis through inflammatory and immunologic mechanisms that lead to the formation of macrophage foam cells.
- Macrophage Foam Cells: These cells are formed when macrophages ingest oxLDL, contributing to plaque formation in the arteries.
The Role of oxLDL in Atherosclerosis:
The oxidation of LDL triggers a cascade of events that lead to atherosclerosis, the hardening and narrowing of arteries. This process involves:
- Inflammation: oxLDL triggers an inflammatory response in the arterial walls.
- Immune Response: The immune system recognizes oxLDL as foreign, further contributing to inflammation.
- Macrophage Recruitment: Macrophages are recruited to the site of inflammation to engulf the oxLDL.
- Foam Cell Formation: When macrophages ingest large amounts of oxLDL, they transform into foam cells.
- Plaque Formation: Foam cells accumulate in the artery walls, contributing to the formation of atherosclerotic plaques.
| Feature | Description |
|---|---|
| Lipid Peroxidation | The oxidation of lipids within the LDL particle. |
| ApoB Modification | Changes to the apolipoprotein B component of LDL. |
| Atherosclerosis | A disease where plaque builds up inside arteries, leading to hardening and narrowing, potentially causing heart disease. |
| Foam Cells | Macrophages that have ingested large amounts of oxLDL, contributing to plaque formation. |
