线粒体病理生理学中的亲环素D
Cyclophilin D in mitochondrial pathophysiology.
作者信息
Giorgio Valentina, Soriano Maria Eugenia, Basso Emy, Bisetto Elena, Lippe Giovanna, Forte Michael A, Bernardi Paolo
机构信息
Department of Biomedical Sciences and CNR Institute of Neuroscience, University of Padova, Italy.
出版信息
Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):1113-8. doi: 10.1016/j.bbabio.2009.12.006. Epub 2009 Dec 21.
Abstract
Cyclophilins are a family of peptidyl-prolyl cis-trans isomerases whose enzymatic activity can be inhibited by cyclosporin A. Sixteen cyclophilins have been identified in humans, and cyclophilin D is a unique isoform that is imported into the mitochondrial matrix. Here we shall (i) review the best characterized functions of cyclophilin D in mitochondria, i.e. regulation of the permeability transition pore, an inner membrane channel that plays an important role in the execution of cell death; (ii) highlight new regulatory interactions that are emerging in the literature, including the modulation of the mitochondrial F1FO ATP synthase through an interaction with the lateral stalk of the enzyme complex; and (iii) discuss diseases where cyclophilin D plays a pathogenetic role that makes it a suitable target for pharmacologic intervention.
摘要
亲环蛋白是一类肽基脯氨酰顺反异构酶，其酶活性可被环孢素A抑制。已在人类中鉴定出16种亲环蛋白，亲环蛋白D是一种独特的异构体，可导入线粒体基质。在此，我们将：（i）回顾亲环蛋白D在线粒体中最具特征的功能，即调节通透性转换孔，这是一种在内膜通道中发挥重要作用的细胞死亡执行过程；（ii）强调文献中出现的新的调节相互作用，包括通过与酶复合物的侧柄相互作用来调节线粒体F1FO ATP合酶；以及（iii）讨论亲环蛋白D发挥致病作用从而使其成为药物干预合适靶点的疾病。
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本文引用的文献
1
Activation of mitochondrial ERK protects cancer cells from death through inhibition of the permeability transition.
Proc Natl Acad Sci U S A. 2010 Jan 12;107(2):726-31. doi: 10.1073/pnas.0912742107. Epub 2009 Dec 22.
2
Cyclophilin D modulates mitochondrial F0F1-ATP synthase by interacting with the lateral stalk of the complex.
J Biol Chem. 2009 Dec 4;284(49):33982-8. doi: 10.1074/jbc.M109.020115. Epub 2009 Sep 29.
3
The changing shape of mitochondrial apoptosis.
Trends Endocrinol Metab. 2009 Aug;20(6):287-94. doi: 10.1016/j.tem.2009.03.007. Epub 2009 Jul 31.
4
The cyclophilin inhibitor Debio 025 normalizes mitochondrial function, muscle apoptosis and ultrastructural defects in Col6a1-/- myopathic mice.
Br J Pharmacol. 2009 Jul;157(6):1045-52. doi: 10.1111/j.1476-5381.2009.00316.x. Epub 2009 Jun 10.
5
Isoform-specific inhibition of cyclophilins.
Biochemistry. 2009 Jul 7;48(26):6268-77. doi: 10.1021/bi9007287.
6
A CaPful of mechanisms regulating the mitochondrial permeability transition.
J Mol Cell Cardiol. 2009 Jun;46(6):775-80. doi: 10.1016/j.yjmcc.2009.03.006. Epub 2009 Mar 19.
7
Genetic ablation of cyclophilin D rescues mitochondrial defects and prevents muscle apoptosis in collagen VI myopathic mice.
Hum Mol Genet. 2009 Jun 1;18(11):2024-31. doi: 10.1093/hmg/ddp126. Epub 2009 Mar 17.
8
The mitochondrial permeability transition pore in motor neurons: involvement in the pathobiology of ALS mice.
Exp Neurol. 2009 Aug;218(2):333-46. doi: 10.1016/j.expneurol.2009.02.015. Epub 2009 Mar 9.
9
Developmental shift of cyclophilin D contribution to hypoxic-ischemic brain injury.
J Neurosci. 2009 Feb 25;29(8):2588-96. doi: 10.1523/JNEUROSCI.5832-08.2009.
10
The molecular composition of the mitochondrial permeability transition pore.
J Mol Cell Cardiol. 2009 Jun;46(6):850-7. doi: 10.1016/j.yjmcc.2009.02.007. Epub 2009 Feb 20.
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