Oxidized LDL-Induced Apoptosis

Conclusion

There is now substantial evidence establishing that oxLDL and lipid peroxidation products generated in the vascular wall, can elicit proinflammatory and pathological events involved in atherosclerosis. As reported by D. Hajjar and M. Haberland, the oxLDL should be considered as true molecular “Trojan Horses” or “cellular saboteurs” bearing a lot of bioreactive products of lipid peroxidation, that modify cell functions, induce intracellular oxidative stress, trigger multiple and contradictatory cell signalings and transcription factors, and finally induce cell death by apoptosis or necrosis. To date, the signaling mechanisms triggered by oxLDL and leading to physiopathological events, are only partly understood. The oxLDL-mediated apoptosis may participate in the progression of atherosclerosis, and in subsequent plaque rupture and thrombotic events which lead finally to acute cardiovascular diseases. In cultured cells antioxidants inhibit LDL oxidation and biological effect of oxLDL, such as apoptosis induction, but their ability to prevent efficiently vascular diseases and to induce regression of established lesions remains to be established. In conclusion, it is very important to clarify the mechanisms of cell-mediated LDL oxidation, as well as the cellular dysfunctions induced by lipid peroxidation products, in order to define new therapeutic strategies efficient in blocking and preventing the atherosclerotic process which always represent a major cause of death in western countries.