Abstract
Mitochondria are dynamic organelles that undergo constant fission and fusion. Mitochondria dysfunction underlies several human disorders, including Alzheimer’s disease (AD). Preservation of mitochondrial dynamics is fundamental for regulating the organelle’s functions. Several proteins participate in the regulation of mitochondrial morphology and networks, and among these, Mitofusin 2 (Mfn2) has been extensively studied. This review focuses on the role of Mfn2 in mitochondrial dynamics and in the crosstalk between mitochondria and the endoplasmic reticulum, in particular in AD. Understanding how this protein may be related to AD pathogenesis will provide essential information for the development of therapies for diseases linked to disturbed mitochondrial dynamics, as in AD.
Highlights
Mitochondria are the power plants of the cell
This review focuses on the role of Mitofusin 2 (Mfn2) in mitochondrial dynamics and in the crosstalk between mitochondria and the endoplasmic reticulum, in particular in Alzheimer’s disease (AD)
Understanding how this protein may be related to AD pathogenesis will provide essential information for the development of therapies for diseases linked to disturbed mitochondrial dynamics, as in AD
Summary
Mitochondria are the power plants of the cell. These organelles are involved in the synthesis of adenosine triphosphate (ATP), and they are responsible for the balance of nutrient storage for energy production. Mitochondria have a fundamental role in the preservation of the cell’s redox balance [1] In the cell, these organelles form a dynamic and connected system in association with the endoplasmic reticulum (ER), which is biochemically and physically linked with the outer membrane of mitochondria (OMM). Among the numerous proteins involved in the link between ER and mitochondria, mitofusin-1 and -2 (Mfn and Mfn2), inositol 1,4,5-triphosphate receptor 3 (IP3R3), and voltage-dependent anion channel 1 (VDAC1) undoubtedly play key roles [3,4] While both Mfn and Mfn occur in the OMM, only Mfn is located in the MAM [5]. Considering the key role of oxidative stress in AD progression and mitochondrial dysfunction, the aim of the present review is to outline the recent knowledge about the role of the fusion protein Mfn in AD onset and evolution
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