Repositori URV

Identificador: TDX:608

Handle: https://hdl.handle.net/20.500.11797/TDX608

Autors:
Cabré Llobet, Anna

Resum:
Atherosclerosis is a progressive disease characterized by an accumulation of lipids in the subendothelial wall. Experimental evidence suggest that lipid peroxidation, inflammatory response and thrombogenic processes play an important role in the pathogenesis of atherosclerosis and its clinical complications. Oxidized LDL particles, some of their oxidative compounds, elevated levels of proinflammatory cytokines and tissue factor (the main inducer of thrombosis) have been detected in plasma of patients with high cardiovascular risk. It has also been reported the presence of all these components in human atherosclerotic plaques where also has been observed an accumulation of inflammatory cells. However, no direct evidence exist about a direct relation between lipid peroxidation and inflammation. A recent interesting finding is the possible role of PPAR in atherosclerosis. PPAR is the nuclear receptor target of thiazolidinediones, drugs used in the treatment of non insulin dependent diabetes mellitus. These drugs have shown a net antiatherosclerotic effect in animal models and in clinical studies in humans. In vitro experiments have shown that thiazolidinediones may have an important antiinflammatory action. PPAR is overexpressed in atherosclerotic plaques where colocalizes with oxidized lipids. Recently, oxidized LDL has been pointed as an important source of PPAR ligands.The work presented in this thesis shows new knowledge of the lipid peroxidation role in the pathogenesis of atherosclerosis emphasized in the action on inflammation and thrombosis. In summary, the obtained results support the theory that lipid oxidative modification plays an important role in the progression of atherothrombotic disease.Results show that the apolar aldehyde