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, 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 from a physical, chemical and biochemical point of view, the
often 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, both diverging outcomes resulting from drug induced modification
of mitochondrial homeostasis.
The aim of this book is to stimulate a re-evaluation of the potential clinical role of mitochondria
that could shed new light on some yet debated aspects of human pathophysiology
|Numero di pagine||492|
|Stato di pubblicazione||Pubblicato - 2012|
|Nome||ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY|