Structural and functional link between the mitochondrial network and the endoplasmic reticulum

被引：310

作者：

Giorgi, Carlotta ^{[1
,2
,3
,4
]}

De Stefani, Diego ^{[1
,2
]}

Bononi, Angela ^{[1
,2
]}

Rizzuto, Rosario ^{[5
]}

Pinton, Paolo ^{[1
,2
]}

机构：

[1] Univ Ferrara, Dept Expt & Diagnost Med, Sect Gen Pathol, ICSI, I-44100 Ferrara, Italy

[2] Univ Ferrara, Dept Expt & Diagnost Med, Sect Gen Pathol, Emilia Romagna Lab BioPharmaNet, I-44100 Ferrara, Italy

[3] Univ Vita Salute San Raffaele, Ctr Excellence Cell Dev, I-20132 Milan, Italy

[4] IIT Network, Res Unit Mol Neurosci, I-20132 Milan, Italy

[5] Univ Padua, Dept Biomed Sci, I-35100 Padua, Italy

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2009年 / 41卷 / 10期

关键词：

ER: endoplasmic reticulum; Mitochondria; MAM: mitochondria associated membranes; Calcium; ER stress; Apoptosis; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; DEPENDENT ANION CHANNEL; UNFOLDED PROTEIN RESPONSE; APOPTOTIC CELL-DEATH; CA2+ RELEASE; INTRACELLULAR CA2+; OUTER-MEMBRANE; TRISPHOSPHATE RECEPTOR; SIGNALING ORGANELLE; IP3; RECEPTORS;

D O I：

10.1016/j.biocel.2009.04.010

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：

Mitochondrial and endoplasmic reticulum (ER) networks are fundamental for the maintenance of cellular homeostasis and for determination of cell fate under stress conditions. Recent structural and functional studies revealed the interaction of these networks. These zones of close contact between ER and mitochondria called MAM (mitochondria associated membranes) support communication between the two organelles including bioenergetics and cell survival. The existence of macromolecular complexes in these contact sites has also been revealed. In this contribution, we will review: (i) the ER and mitochondria structure and their dynamics, (ii) the basic principles of ER mitochondrial Ca2+ transport, (iii) the physiological/pathological role of this cross-talk. (C) 2009 Elsevier Ltd. All rights reserved.

引用

页码：1817 / 1827

页数：11

共 107 条

[1] The mitochondrial fission protein hFis1 requires the endoplasmic reticulum gateway to induce apoptosis [J].