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چکیده : 

Lipid signaling in disease is an important field of investigation and stems from the pioneering work

from our and Irvine’s laboratories at the end of the eighties (Cocco et al., 1987). Inositides are key

cellular second messengers with well established roles in signal transduction pathways. A distinct

nuclear inositide signaling metabolism has been identified, thus defining a new role for nuclear inositides,

which are now considered essential co-factors for several nuclear processes, including DNA

repair, transcription regulation, and RNA dynamics. Imbalances of the major lipid signaling pathways

may contribute to disease progression in several disorders, such as chronic inflammation, cancer,

metabolic, and degenerative syndromes. Inositide signaling cascades are therefore essential components

of the extremely complicated, multistep process that allows one extracellular signal to be

transduced inside the cell, to the nucleus. Moreover, these pathways are complex and redundant, and

many of the signaling molecules, their modifying enzymes and downstream targets are common to

multiple pathways (Cocco et al., 2009; Faenza et al., 2008; Martelli et al.,1992). As a consequence, many

signaling pathways can be deregulated in several pathological conditions, as well as in cancer. That is

why several signaling lipid-generating enzymes have been and are still being targeted pharmacologically,

alone or in combination, to alleviate the symptoms, or even progression of the different diseases

(Cocco et al., 2010; Wymann and Schneiter, 2008).