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Abstract:
Apoptosis – a regulated form of cell death – is the main mode of cell death in most liver injuries. Mitochondria, besides their recognized role as energy-providing metabolic centers, are also key regulatory centers during the genesis of apoptosis. Consequently, increasing interest has developed around the relations between cell metabolism and cell death/survival. We have recently shown that
the initial phase of the apoptotic process is associated with alterations in specific glucose metabolic pathways.
The synthetic glucocorticoid Dexamethasone (DEX) is a commonly used therapeutic agent in several inflammatory disorders.
Besides its clinical use, DEX is known to inhibit apoptosis in vitro. So far, the exact underlying mechanisms of the anti-apoptotic effect of DEX are poorly understood and are currently being investigated.[1,2] Interestingly, with regards to our earlier observations DEX has been shown to modify metabolic pathways (in particular, anaplerosis and gluconeogenesis) both in vivo and in vitro.
