Mitochondrial Membrane Lipids in Life and Death and their Molecular Modulation by Diet: Tuning the Furnace

心磷脂 线粒体 细胞生物学 线粒体内膜 膜接触部位 生物 细胞器 内质网 磷脂 细菌外膜 生物膜 生物化学 化学 膜蛋白 整体膜蛋白 基因 大肠杆菌
作者
João P. Monteiro,Catarina M. Morais,Paulo J. Oliveira,Amália S. Jurado
出处
期刊:Current Drug Targets [Bentham Science]
卷期号:15 (8): 797-810 被引量:10
标识
DOI:10.2174/1389450115666140623115315
摘要

The traditional view of mitochondria as cell powerhouses is a matter of common knowledge, but the overall view of these extraordinary organelles has been revolutionized in the last years. In fact, a large number of important and diverse processes take place at the mitochondrial level, which clearly surpass the energy production scope, intruding the critical fragile balance between cell life and death. The entangled biochemistry of mitochondrial membranes has been found to be dependent on specific lipid requirements, with cardiolipin holding a great part of the raised functional interest. Mitochondria contain a complex membrane system, based on a variety of lipids and exquisite asymmetries. Mitochondria lipid membrane composition depends on a tight interplay with the endoplasmic reticulum, from which some of the lipids present in the mitochondrial membranes have to be imported, at least in the form of precursors. Here, we review some external interventions resulting in alterations of mitochondrial lipid content, namely dietary interventions and genetic manipulation. Such manipulations of mitochondrial membrane lipid composition should result in physiological impact, given the importance of lipid-protein interactions within the mitochondrial membrane boundaries. We provide arguments for future experiments using the most modern chemical and biophysical approaches as well as computer simulation studies applied to appropriate biological membrane model systems, in order to identify the effects exerted by diet-induced lipid changes on membrane physical properties. Keywords: Apoptosis, cardiolipin, diet, lipid-protein interactions, membrane lipid remodelling, mitochondrial membrane asymmetries, mitochondrial phospholipid synthesis.
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