Research press release


Nature Medicine

A stroke against stroke


脳血管障害後のニューロン死の主な原因は、脳の興奮性受容体が過剰に活性化されることによる損傷である。このような受容体の中で特にカギを握るのが、いわゆるNMDA型グルタミン酸受容体である。Y T Wangたちは、マウスの脳血管障害でのNMDA型受容体を介したニューロン死にはSREBP-1とよばれる分子の活性化が不可欠なことを明らかにした。


A new cellular mechanism linked to neuronal damage during stroke is reported this week in Nature Medicine. Targeting this mechanism may have therapeutic potential in people.

Damage caused by overactivation of excitatory receptors in the brain is a principal cause of neuronal loss after stroke. Among these receptors, the so-called NMDA subtype of glutamate receptors is a key player. Yu Tian Wang and his team found that activation of a molecule called SREBP-1 in affected neurons is an essential step in NMDA receptor-mediated neuronal death in stroke in mice.

According to the authors, the activation of SREBP-1 is linked to the loss of a known SREBP-1 binding partner known as Insig-1. Using a compound capable of inhibiting the loss of Insig-1, the team could interfere with SREBP-1 activation, and therefore reduce neuronal damage and prevent neurological deficits after stroke in mice. This highlights the potential of agents that reduce SREBP-1 activation in cases of stroke.

doi: 10.1038/nm.2064


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