Advances in Mitochondrial Medicine
Roberto Scatena, Patrizia Bottoni, Bruno Giardina
Springer Science & Business Media, Feb 9, 2012 - Medical - 461 pages
Mitochondria are far more than the “powerhouse” of the cell as they have classically been described. In fact, mitochondria biological activities have progressively expanded to include not only various bioenergetic processes but also important biosynthetic pathways, calcium homeostasis and thermogenesis, cell death by apoptosis, several different signal transduction pathways mainly related to redox control of gene expression and so on. This functional and structural complexity may undergo important derangements so to justify the definition of ‘mitochondrial medicine’, which should include all the clinical consequences of congenital or acquired mitochondrial dysfunctions. There are actually a growing number of studies which assign a significant pathogenic role to damaged mitochondria in different diseases: ischemia/reperfusion injury, neurodegenerative diseases, cancer with its dramatic sequelae (i.e, metastasis), metabolic syndrome, hyperlipidemias, just to mention a few of the most important pathologies. In this context, a further aspect that should not be disregarded is the interaction of pharmacological agents with mitochondria, not only in regard of the toxicological aspects but, above all, of the potential therapeutic applications. In fact, it is interesting to note that, while the properties of different so-called “mitoxicants” are well-known, the subtle linkages between drugs and mitochondria is still in need of a real pharmacological and therapeutic control at the clinical level. This lack of consideration can often lead to an underestimation of unwanted toxic effects but also of desirable therapeutic activities. A reevaluation of the potential clinical role of mitochondria could give a new light on some yet obscure aspects of human pathophysiology.
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Acad Sci USA acid activity aging anthracyclines antioxidant apoptosis apoptotic ATP synthase Biochem Biochim Biophys Acta Biol Chem cancer cells cardiac cardiomyopathy cardiotoxicity caspase Cell Biol cell death cellular chondrial clinical Complex III cytochrome c oxidase cytosolic decrease deﬁciency dehydrogenase deletions diabetes drial drugs electron encoded enzyme ﬁbers ﬁrst Free Radic gene Genet genome heart human identiﬁed increased induced inhibition inhibitors insulin resistance interaction kinase levels lipid mammalian mechanism metabolism mice mito mitochon mitochondrial Caz mitochondrial DNA mitochondrial dysfunction mitochondrial function mitochondrial membrane mitochondrial proteins mitochondrial toxicity molecular mtDNA mtDNA mutations NADH Natl Acad Sci neurons nitric oxide NRTIs nuclear nucleotide oxidative damage oxidative phosphorylation oxidative stress OXPHOS pathway patients peroxide Physiol Proc Natl Acad proteomic proton reactive oxygen species redox reduced regulation respiration respiratory chain role ROS production signalling signiﬁcant skeletal muscle speciﬁc studies subunits superoxide syndrome target tissues transport tumour UCP1 uncoupling protein