SR/ER-mitochondrial local communication: Calcium and ROS

被引:240
作者
Csordas, Gyoergy [1 ]
Hajnoczky, Gyoergy [1 ]
机构
[1] Thomas Jefferson Univ, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2009年 / 1787卷 / 11期
关键词
Superoxide anion; H2O2; IP3; receptor; Ryanodine receptor; SERCA; Bioenergetics; Apoptosis; ALPHA-KETOGLUTARATE DEHYDROGENASE; PERMEABILITY TRANSITION PORE; PROTEIN-KINASE-C; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR-TYPE-1; CHANNEL RYANODINE RECEPTOR; ENDOPLASMIC-RETICULUM; OXIDATIVE STRESS; SARCOPLASMIC-RETICULUM; REDOX REGULATION; CA2+ UPTAKE;
D O I
10.1016/j.bbabio.2009.06.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondria form junctions with the sarco/endoplasmic reticulum (SR/ER), which support signal transduction and biosynthetic pathways and affect organellar distribution. Recently, these junctions have received attention because of their pivotal role in mediating calcium signal propagation to the mitochondria, which is important for both ATP production and mitochondrial cell death. Many of the SR/ER-mitochondrial calcium transporters and signaling proteins are sensitive to redox regulation and are directly exposed to the reactive oxygen species (ROS) produced in the mitochondria and SR/ER. Although ROS has been emerging as a novel signaling entity, the redox signaling of the SR/ER-mitochondrial interface is yet to be elucidated. We describe here possible mechanisms of the mutual interaction between local Ca2+ and ROS signaling in the control of SR/ER-mitochondrial function. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:1352 / 1362
页数:11
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