Functional implications of mitofusin 2-mediated mitochondrial-SR tethering.
作者： Gerald W. Dorn , Moshi Song , Kenneth Walsh
DOI: 10.1016/J.YJMCC.2014.09.015
关键词: Mitochondrial membrane transport protein 、 MFN2 、 Calcium signaling 、 Mitofusin-2 、 Mitochondrial permeability transition pore 、 MFN1 、 mitochondrial fusion 、 Mitochondrion 、 Biology 、 Cell biology
摘要: Cardiomyocyte mitochondria have an intimate physical and functional relationship with sarcoplasmic reticulum (SR). Under normal conditions mitochondrial ATP is essential to power SR calcium cycling that drives phasic contraction/relaxation, changes in release are sensed by used modulate oxidative phosphorylation according metabolic need. When perturbed, mitochondrial-SR crosstalk can evoke programmed cell death. Physical proximity interplay between maintained part through tethering of these two organelles the membrane protein mitofusin 2 (Mfn2). Here we review discuss findings from our laboratories derive genetic manipulation Mfn2 closely related Mfn1 mouse hearts other experimental systems. By comparing independent research efforts arrive at several conclusions appear be strongly supported, describe a few areas incomplete understanding will require further study. In so doing hope clarify some misconceptions regarding many varied roles as both trans-organelle tether fusion protein. This article Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology Cardiovascular Disease."
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