The mechanisms of mitochondrial dysfunction development in vessels upon peroxodized LDL (pLDL) influence are discussed. Is is shown that the components of pLDL induce the formation of covalent complexes with cell proteins and destabilize cellular membrane microdomain structure that leads to membrane proteins dysfunction, Ca2+ liberation into cytosol from its stores, endoplasmic reticulum stress, increase in reactive oxygen species production by NADPH-oxidases. These effects cause disturbances in mitochondria of target cells, increases in reactive oxygen species production, mitochondrial pathway of cell death. The processes under discussion contribute to the atherosclerotic leisure development.
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