Journal ArticleDOI
The regulation of mitochondrial morphology: intricate mechanisms and dynamic machinery.
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TLDR
This review focuses on the current understanding of the mitochondrial morphology machinery in cell homeostasis, apoptosis and neurodegeneration, and the post translational modifications that regulate these processes.About:
This article is published in Cellular Signalling.The article was published on 2011-10-01. It has received 252 citations till now. The article focuses on the topics: mitochondrial fusion & Mitochondrion.read more
Citations
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Mitochondrial rhomboid parl regulates cytochrome c release during apoptosis via OPA1 dependent cristae remodeling
Sara Cipolat,Tomasz Rudka,Dieter H. Hartmann,Costa,S. Serneels,Kathleen Craessaerts,Kristine Metzger,Luca Scorrano,Bart De Strooper +8 more
TL;DR: Parl-associated rhomboid-like (PARL-like) as mentioned in this paper is an inner mitochondrial membrane rhomboids of unknown function, whose yeast ortholog is involved in mitochondrial fusion.
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hFis1, a novel component of the mammalian mitochondrial fission machinery. Vol. 278 (2003) 36373–36379
TL;DR: In this article, the authors identified a mammalian protein called hFis1, which is the orthologue of the yeast Fis1p known to participate in yeast mitochondrial division, and when overexpressed in various cell types, localized to the outer mitochondrial membrane and induced mitochondrial fission.
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Bioenergetic role of mitochondrial fusion and fission.
TL;DR: Fragmented mitochondria are frequently found in resting cells, and mitochondrial fission plays an important role in the removal of damaged organelles by autophagy, which contributes to maintenance of mitochondrial function and optimize bioenergetic capacity.
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Cellular and molecular mechanisms of mitochondrial function
TL;DR: Mitochondria are membrane bound organelles present in almost all eukaryotic cells and contribute to many processes central to cellular function and dysfunction including calcium signalling, cell growth and differentiation, cell cycle control and cell death.
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Impaired mitochondrial function in psychiatric disorders.
Husseini K. Manji,Tadafumi Kato,Nicholas A. Di Prospero,Seth Ness,M. Flint Beal,Michael Krams,Guang Chen +6 more
TL;DR: There is a growing body of evidence to suggest that impaired mitochondrial function may affect key cellular processes, thereby altering synaptic functioning and contributing to the atrophic changes that underlie the deteriorating long-term course of these illnesses.
References
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Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice
Naotada Ishihara,Masatoshi Nomura,Akihiro Jofuku,Hiroki Kato,Satoshi O. Suzuki,Keiji Masuda,Hidenori Otera,Yae Nakanishi,Ikuya Nonaka,Yu-ichi Goto,Naoko Taguchi,Hidetaka Morinaga,Maki Maeda,Ryoichi Takayanagi,Sadaki Yokota,Katsuyoshi Mihara +15 more
TL;DR: Drp1−/− murine embryonic fibroblasts and embryonic stem cells revealed that Drp1 is required for a normal rate of cytochrome c release and caspase activation during apoptosis, although mitochondrial outer membrane permeabilization, as examined by the release of Smac/Diablo and Tim8a, may occur independently of Drp 1 activity.
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Reversible phosphorylation of Drp1 by cyclic AMP-dependent protein kinase and calcineurin regulates mitochondrial fission and cell death
J. Thomas Cribbs,Stefan Strack +1 more
TL;DR: Drp1 phosphorylation at Ser 656 provides a mechanism for the integration of cAMP and calcium signals in the control of mitochondrial shape, apoptosis and other aspects of mitochondrial function.
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Mitochondria take center stage in aging and neurodegeneration
TL;DR: There is strong evidence from genetics and transgenic mouse models that mitochondrial dysfunction results in neurodegeneration and may contribute to the pathogenesis of Alzheimer’s disease, Parkinson's disease, Huntington's Disease, amyotrophic lateral sclerosis, hereditary spastic paraplegia, and cerebellar degenerations.
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Mitochondrial Fusion and Fission in Mammals
TL;DR: Key components of the mitochondrial fusion and fission machinery have been identified, allowing initial dissection of their mechanisms of action, which play important roles in mitochondrial function and development as well as programmed cell death.
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Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission
Ruben K. Dagda,Salvatore J. Cherra,Scott M. Kulich,Scott M. Kulich,Anurag Tandon,David S. Park,Charleen T. Chu +6 more
TL;DR: It is found that loss of PINK1 function elicits oxidative stress and mitochondrial turnover coordinated by the autophagic and fission/fusion machineries, and Pink1 and Parkin may cooperate through different mechanisms to maintain mitochondrial homeostasis.