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uonderuoman.
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se qualche volontario puo fare un sunto traduzione lo ringrazio di cuore.
http://www.autismcalciumchannelopathy.com/...chondrial.html#
d questa parte:
Calcium homeostasis and mitochondria
One of the functions of mitochondria is to store free calcium. Release of this stored calcium back into the interior of the cell can initiate calcium spikes or waves. These events coordinate various processes in different types of cells, for example neurotransmitter release in nerve cells and release of hormones in endocrine cells. Excess calcium ions stored in mitochondria can inhibit oxidative phosphorylation. In the nerve cells this can causes an irreversible reduction in the energy status of nerve terminals, which can initiate pathophysiological processes in those cells.
Numerous findings have indicated a crucial role of calcium influx through L-type calcium channels in mitochondrial calcium overload and downstream mitochondrial and cellular dysfuctions. It has been shown that blockade of LTCC in the plasma membrane not only inhibits an increase in cellular calcium but also stabilizes mitochondrial membranes calcium homeostasis and generation of ROS by mitochondria [16760264, 11746731]. In one study inhibition of calcium inward current with verapamil protected against oxidative stress as well as morphological changes and dysfunction of mitochondria [16644187] (Oxidative_Stress). There are some indications that, simultanious to LTCC, N-methyl-D-aspartate (NMDA) receptors are also involved in oxidative stress, mitochondrial dysfunction, and ATP depletion mediated by calcium influx [12473387].
The involvement of LTCC in cellular and mitochondrial accumulation of calcium has been demonstrated in vitro in hypoxic renal tubular cells [15339981], and in bovine chromaffin cells [11500491], showing that these channels play an important role in regulating mitochondrial permeability transition, cytochrome c release, caspase activation, and ATP depletion-induced mitochondrial apoptosis. The reduced efficiency of handling of intracellular calcium loads in neurons may be an important factor contributing to the onset of neuronal damage during hypoxia and ischaemia [8012725]. Calcium influx through LTCC is involved in the ischemic damage in neonatal brain which manifests itself as a decrease in the energy state, with decreased levels of phosphocreatine and ATP, and an increases in lactate [88974726] (see Hypoxia/Ischemia).
At the same time deenergization of mitochondria affects the cellular calcium influx rate [10930575]. Several inherited human encephalomyopathies exhibit neurological symptoms, including autism-related symptoms, in association with specific mitochondrial mutations [7846043]. It can therefore be proposed that this inability to regulate calcium influx and homeostasis is one of the probable mechanisms behind increased neuronal vulnerability and subsequent development of autistic-like behavioural symptoms in human encephalomyopathies..
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