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Electronegative low-density lipoprotein.
José Luis Sánchez-Quesada1, Sonia Benítez, Jordi Ordóñez-Llanos
1Biochemistry Department and Research Institute, Hospital de la Santa Creu i Sant Pau, C/Antoni Maria Claret 167, 08025 Barcelona, Spain.
Current Opinion in Lipidology
|May 29, 2004
Summary
Electronegative LDL (LDL(-)) shows new evidence of contributing to atherosclerosis. This LDL subtype promotes inflammation, apoptosis, and impaired angiogenesis, suggesting a significant role in cardiovascular disease development.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Immunology
Background:
- Electronegative LDL (LDL(-)) was identified in 1988, but its atherogenic role remained controversial through the 1990s.
- Recent research has provided compelling evidence for the atherogenic potential of LDL(-).
Purpose of the Study:
- This review synthesizes recent findings on the atherogenic role of LDL(-).
- To discuss the mechanisms by which LDL(-) contributes to atherosclerosis.
Main Methods:
- Review of recent scientific literature on LDL(-).
- Analysis of studies investigating LDL(-) effects on endothelial cells and related molecular pathways.
Main Results:
- LDL(-) induces chemokine production (IL-8, MCP-1) and enhances TNF-alpha-induced VCAM-1 expression in endothelial cells, promoting leukocyte recruitment.
- LDL(-) from familial hypercholesterolemic patients impairs angiogenesis and increases apoptosis by decreasing DNA synthesis and FGF2 production.
- Platelet-activating factor acetylhydrolase preferentially associates with LDL(-), indicating a proinflammatory role.
Conclusions:
- Recent evidence suggests LDL(-) contributes to atherogenesis through proinflammatory, proapoptotic, and anti-angiogenic mechanisms.
- Further research is needed to fully elucidate the role of LDL(-) in atherogenesis and endothelial cell activation.