Molecular Mechanisms of Interactions between Mitochondria and the Endoplasmic Reticulum: A New Look at How Important Cell Functions are Supported

被引:0
作者
Sukhorukov, V. S. [1 ]
Voronkova, A. S. [1 ]
Baranich, T., I [1 ,2 ]
Gofman, A. A. [2 ]
Brydun, A., V [1 ,2 ]
Knyazeva, L. A. [2 ]
Glinkina, V. V. [2 ]
机构
[1] Neurol Res Ctr, Moscow 125367, Russia
[2] Pirogov Russian Natl Res Med Univ, Moscow 117997, Russia
关键词
endoplasmic reticulum; mitochondria; membrane; calcium; chaperone; neurodegenerative diseases; DEPENDENT ANION CHANNEL; MEMBRANE MAM INTEGRITY; ER MEMBRANES; MOUSE MODEL; MITOFUSIN; CA2+; CALCIUM; STRESS; DISEASE; PARKINSONS;
D O I
10.1134/S0026893322010071
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
Interactions between the endoplasmic reticulum (ER) and mitochondria have received insufficient attention until recently. However, distorted contacts between the ER and mitochondria were identified as an important factor in the etiopathogenesis of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. In view of these new data, the mechanisms of ER-mitochondrial interactions are necessary to study in detail in order to develop new diagnostic and therapeutic approaches to neurodegenerative diseases and to extend basic knowledge of the physiology of the eukaryotic cell. The review focuses on the functions of mitochondria-associated ER membranes (MAMs). Structural elements of the MAM system, their contributions to the vital cell functions (calcium and lipid homeostasis, autophagy, fusion and division of mitochondria, and the regulation of their number), and the role of MAM dysfunctions in the pathogenesis of various neurodegenerative diseases are considered.
引用
收藏
页码:59 / 71
页数:13
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