Mitochondria produce large amounts of free radicals and play an important role in the life and death of a cell, regulating the signalling, metabolism, and energy production needed for cellular function. In this way, mitochondrial oxidative damage and dysfunction contribute to a number of cell pathologies that are manifested through a range of conditions that include cardiovascular diseases (CVD). Although the molecular mechanisms responsible for mitochondriamediated disease processes are not yet completely understood, oxidative stress definitely seems to play an important role. When examined at the protein level, both expression levels and protein modifications are altered by oxidative stress. While these effects have been studied in the past by classic biochemical methods, recent developments in proteomics have allowed the oxidative stress response to be studied in more depth. The focus of this work is the mitochondrial proteome/ genome interplay that is currently believed to be implicated in a range of human diseases. Particular attention is given to the current knowledge of the role of mitochondria in the development of oxidative-stress-based diseases; e.g. CVD is highlighted together with the prospective proteomics perspective as an alternative prognostic and diagnostic tool for interpreting many mitochondria-related anomalies. Accordingly, strategies for the targeted delivery of antioxidants to mitochondria are being developed. The insight provided by recent proteomic research and the effects of mitochondrialantioxidants on possible interventions are also discussed.
Keywords: Antioxidant, cardiovascular disease, free radicals, mitochondria, oxidative stress, proteomics
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