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首页> 外文期刊>Protoplasma: An International Journal of Cell Biology >Nanospaces between endoplasmic reticulum and mitochondria as control centres of pancreatic β-cell metabolism and survival
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Nanospaces between endoplasmic reticulum and mitochondria as control centres of pancreatic β-cell metabolism and survival

机译：内质网和线粒体之间的纳米空间作为胰腺β细胞代谢和存活的控制中心

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摘要

Nanometre-scale spaces between organelles represent focused nodes for signal transduction and the control of cellular decisions. The endoplasmic reticulum (ER) and the mitochondria form dynamic quasi-synaptic interaction nanodomains in all cell types examined, but the functional role of these junctions in cellular metabolism and cell survival remains to be fully understood. In this paper, we review recent evidence that ER Ca ~(2+) channels, such as the RyR and IP _3R, can signal specifically across this nanodomain to the adjacent mitochondria to pace basal metabolism, with focus on the pancreatic β-cell. Blocking these signals in the basal state leads to a form of programmed cell death associated with reduced ATP and the induction of calpain-10 and hypoxia-inducible factors. On the other hand, the hyperactivity of this signalling domain plays a deleterious role during classical forms of apoptosis. Thus, the nanospace between ER and mitochondria represents a critical rheostat controlling both metabolism and programmed cell death. Many aspects of the mechanisms underlying this control system remain to be uncovered, and new nanotechnologies are required understand these domains at a molecular level.
机译：细胞器之间的纳米级空间代表信号转导和细胞决策控制的聚焦节点。内质网（ER）和线粒体在所有检查的细胞类型中形成动态的拟突触相互作用纳米域，但这些连接在细胞代谢和细胞存活中的功能作用尚待充分了解。在本文中，我们回顾了最近的证据，即ER Ca〜（2+）通道（例如RyR和IP _3R）可以通过该纳米域向邻近的线粒体发出特定信号，以加快基础代谢，重点是胰腺β细胞。在基础状态下阻断这些信号会导致某种形式的程序性细胞死亡，这种细胞死亡与ATP降低以及calpain-10和缺氧诱导因子的诱导有关。另一方面，该信号结构域的过度活跃在经典形式的细胞凋亡期间起有害作用。因此，内质网与线粒体之间的纳米空间代表了控制代谢和程序性细胞死亡的关键变阻器。该控制系统的基础机制的许多方面仍有待发现，并且需要新的纳米技术从分子水平上理解这些领域。

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