By Sergio Papa, Pietro Luca Martino, Giuseppe Capitanio, Antonio Gaballo (auth.), Roberto Scatena, Patrizia Bottoni, Bruno Giardina (eds.)
Mitochondria are excess of the “powerhouse” of the mobile as they've got classically been defined. actually, mitochondria organic actions have gradually increased to incorporate not just numerous bioenergetic techniques but additionally very important biosynthetic pathways, calcium homeostasis and thermogenesis, cellphone dying through apoptosis, a number of varied sign transduction pathways customarily regarding redox keep an eye on of gene expression etc. This useful and structural complexity may perhaps suffer very important derangements so that you can justify the definition of ‘mitochondrial medicine’, which may still comprise all of the scientific results of congenital or bought mitochondrial dysfunctions. There are literally increasingly more experiences which assign an important pathogenic function to broken mitochondria in several ailments: ischemia/reperfusion damage, neurodegenerative illnesses, melanoma with its dramatic sequelae (i.e, metastasis), metabolic syndrome, hyperlipidemias, simply to point out many of the most crucial pathologies. during this context, one more point that are meant to no longer be skipped over is the interplay of pharmacological brokers with mitochondria, not just in regard of the toxicological points yet, especially, of the aptitude healing functions. actually, it truly is fascinating to notice that, whereas the houses of alternative so-called “mitoxicants” are recognized, the sophisticated linkages among medicinal drugs and mitochondria remains to be wanting a true pharmacological and healing keep watch over on the medical point. This loss of attention can frequently result in an irony of undesirable poisonous results but in addition of fascinating healing actions. A reevaluation of the capability scientific function of mitochondria may supply a brand new gentle on a few but imprecise elements of human pathophysiology.
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Proteomics 7(10):1575–1583 Panke O, Gumbiowski K, Junge W, Engelbrecht S (2000) F-ATPase: specific observation of the rotating c subunit oligomer of EF(O) EF(1). FEBS Lett 472:34–38 Papa S (1976) Proton translocation reactions in respiratory chains. Biochim Biophys Acta 456:39–84 Papa S (1996) Mitochondrial oxidative phosphorylation changes in the life span. Molecular aspects and physiopathological implications. Biochim Biophys Acta 1276:87–105 Papa S (2002) The NDUFS4 nuclear gene of complex I of mitochondria and the cAMP cascade.
FEBS Lett 472:34–38 Papa S (1976) Proton translocation reactions in respiratory chains. Biochim Biophys Acta 456:39–84 Papa S (1996) Mitochondrial oxidative phosphorylation changes in the life span. Molecular aspects and physiopathological implications. Biochim Biophys Acta 1276:87–105 Papa S (2002) The NDUFS4 nuclear gene of complex I of mitochondria and the cAMP cascade. Biochim Biophys Acta 1555:147–153 Papa S, Skulachev VP (1997) Reactive oxygen species, mitochondria, apoptosis and aging. Mol Cell Biochem 174:305–319 Papa S, Lofrumento NE, Quagliariello E, Meijer AJ, Tager JM (1971) Coupling mechanisms in anionic substrate transport across the inner membrane of rat-liver mitochondria.
In humans, the search for the nuclearly encoded mitochondrial proteins has been further boosted by studies on mitochondrial disorders. More recently, the identification of mitochondrial proteins has benefited of global approaches in the fields of comparative genomics and proteomics for human mitochondria (Taylor et al. 2003b; Cotter et al. 2004), and for other model organisms (Mootha et al. 2003; Premsler et al. 2009). For description of mtDNA structure, expression and genetics see the following chapter by Ian Holt.