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 phone as they've got classically been defined. actually, mitochondria organic actions have gradually improved to incorporate not just quite a few bioenergetic procedures but additionally vital biosynthetic pathways, calcium homeostasis and thermogenesis, cellphone demise by means of apoptosis, a number of diversified sign transduction pathways regularly regarding redox keep an eye on of gene expression etc. This sensible and structural complexity could suffer vital derangements so that you could justify the definition of ‘mitochondrial medicine’, which should still comprise all of the scientific results of congenital or got mitochondrial dysfunctions. There are literally more and more reports which assign an important pathogenic function to broken mitochondria in numerous illnesses: ischemia/reperfusion damage, neurodegenerative ailments, melanoma with its dramatic sequelae (i.e, metastasis), metabolic syndrome, hyperlipidemias, simply to point out some of the most crucial pathologies. during this context, another element that are meant to no longer be skipped over is the interplay of pharmacological brokers with mitochondria, not just in regard of the toxicological facets yet, specifically, of the capability healing functions. in reality, it's attention-grabbing to notice that, whereas the houses of alternative so-called “mitoxicants” are recognized, the delicate linkages among medicines and mitochondria continues to be wanting a true pharmacological and healing keep an eye on on the scientific point. This loss of attention can frequently bring about a sarcasm of undesirable poisonous results but additionally of fascinating healing actions. A reevaluation of the capability medical position of mitochondria may perhaps supply a brand new mild on a few but vague facets of human pathophysiology.
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Extra info for Advances in Mitochondrial Medicine
Various human mitochondrial diseases are caused by mutations in the mitochondrial gene encoding the ATP synthase subunit a, such Leber’s hereditary optic neuropathy (LHON), the maternally inherited Leigh syndrome (MILS) and the neurogenic ataxia and retinitis pigmentosa (NARP) (reviewed in Kucharczyk et al. 2009 and references therein). 4 Biogenesis of Oxidative Phosphorylation Complexes Biogenesis of mitochondria involves the formation of the organelle during the cell life cycle (Attardi and Schatz 1988; Leaver and Lonsdale 1989).
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Activation of protein kinases by cAMP and/or Ca2+ results in phosphorylation of CREB and members of the transducer of regulated CREB binding protein family (TORCs) (Screaton et al. 2004; Bittinger et al. 2004). CREB and TORC together promote the transcription of PGC-1a and cytochrome c genes. The activity and/or expression of PGC-1a responds to a variety positive and negative signal pathways (López-Lluch et al. 2008). The transcriptional level of PGC-1a is also increased by NO. PGC-1a is also activated by post-translational modifications, like deacetylation by SIRT1, phosphorylation by AMPK and P38MAPK and inhibited by phosphorylation by AKT which is activated by insulin pathway.
Advances in Mitochondrial Medicine by Sergio Papa, Pietro Luca Martino, Giuseppe Capitanio, Antonio Gaballo (auth.), Roberto Scatena, Patrizia Bottoni, Bruno Giardina (eds.)