@misc{Suski_Maciej_Liver_2011,
 author={Suski, Maciej},
 address={Kraków},
 howpublished={online},
 year={2011},
 school={Uniwersytet Jagielloński. Collegium Medicum. Wydział Lekarski.},
 language={pol},
 abstract={Despite remarkable progress in modern medicine, atherosclerosis and atherosclerosis-related organ injury are one of the major cause of morbidity in Western countries. Mechanisms responsible for observed organ damage in atherosclerosis (for example in liver and kidneys) are still not well established. However there is a growing body of literature pointing to mitochondrial dysfunctionas a important factor in organ pathology development. The aim of this study was to asses the protein expression changes in liver and kidney mitochondria of atherosclerosis developing apoE-knockout mice and to examine the possible effect of angiotensin-(1-7) peptidemimetic AVE 0991 on mitochondrial proteins alterations. In present work, for the first time the differential proteomic approach was applied to examine mitochondrial protein expression changes related to organ injury caused by atherosclerosis progression and to investigate the possible influence of MAS receptor agonist AVE 0991 on mitoproteom. Study revealed differences in expression of proteins related to antioxidant defense, mitochondrial metabolism and control of apoptosis. Peptidemimetic AVE 0991 altered the protein content –changes may be a hallmark of mechanisms triggered in mitochondria to compensate dysfunction and improve its function. Presented results highlight the key role of mitochondria in maintaining cell homeostasis and point to the importance of developing new pharmacological strategies based on mitochondrial action of new drugs to counteract the organ injury in atherosclerosis.},
 title={Liver and kidney mitochondria proteome changes inatherosclerosis in apoE-knockout mice model},
 type={Praca doktorska},
 keywords={atherosclerosis, liver, kidney, mitochondria, proteomics},
}