Research Reports - The role of mitochondrial calcium uniporter in neuroprotection in traumatic brain injury

Med Hypotheses. 2012 Nov 27

Cheng G, Fu L, Zhang HY, Wang YM, Zhang LM, Zhang JN

The alteration in cellular Ca(2+) homeostasis is one of the key mechanisms
contributing to secondary neuronal damage and altered physiology during the
process of traumatic brain injury (TBI). However, there is considerable
uncertainty about the efficacy of calcium channel blockers in randomized,
controlled, clinical trials. In the physiological condition, cellular Ca(2+)
homeostasis occurs through repetitive bursts of rising intracellular Ca(2+) that,
sometimes are referred to as Ca(2+) oscillations. Mitochondria are intimately
involved in the spatiotemporal tuning of cellular Ca(2+) signaling mainly through
mitochondrial Ca(2+) uniporter (MCU). Excessive Ca(2+) uptake by the mitochondria
through MCU is a key event in mitochondrial dysfunction and cell death in TBI.
Selective inhibition of MCU has showed a promising cardioprotection and
neuroprotection effect in many preclinical studies. Based on these preclinical
results, the selective inhibition of MCU may be a new strategy for
neuroprotection in TBI patients.

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