OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
Christian Frezza,Sara Cipolat,Olga Martins de Brito,Massimo Micaroni,Galina V. Beznoussenko,Tomasz Rudka,Davide Bartoli,Roman S. Polishuck,Nika N. Danial,Bart De Strooper,Luca Scorrano +10 more
TLDR
Evidence is provided that Optic Atrophy 1 (OPA1), a profusion dynamin-related protein of the inner mitochondrial membrane mutated in dominant optic atrophy, protects from apoptosis by preventing cytochrome c release independently from mitochondrial fusion.About:
This article is published in Cell.The article was published on 2006-07-14 and is currently open access. It has received 1444 citations till now. The article focuses on the topics: Optic Atrophy 1 & Inner mitochondrial membrane.read more
Citations
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The Good and the Bad of Mitochondrial Breakups.
TL;DR: Recent advances in the field of mitochondrial dynamics are discussed, demonstrating cell- and tissue-specific effects of mitochondrial fragmentation on cellular metabolism, cell survival, and mitochondrial quality control.
Journal ArticleDOI
Emerging roles of mitochondrial proteases in neurodegeneration.
TL;DR: Current knowledge on how disturbances of the mitochondrial proteolytic system affect neuronal maintenance and axonal function is reviewed.
Journal ArticleDOI
Heterozygous mutation of Opa1 in Drosophila shortens lifespan mediated through increased reactive oxygen species production.
TL;DR: The results, for the first time, demonstrate the important role of OPA1 in aging and lifespan, which is most likely mediated through augmented ROS production.
Journal ArticleDOI
The Mitochondrial Inner Membrane GTPase, Optic Atrophy 1 (Opa1), Restores Mitochondrial Morphology and Promotes Neuronal Survival following Excitotoxicity
Arezu Jahani-Asl,Karine Pilon-Larose,William Xu,Jason G. MacLaurin,David S. Park,Heidi M. McBride,Ruth S. Slack +6 more
TL;DR: Opa1 is suggested as a potential therapeutic target to promote neuronal survival following acute brain damage and neurodegenerative diseases by defining a mechanism whereby breakdown of the mitochondrial network mediated through loss of Opa1 function contributes to neuronal death following excitotoxic neuronal injury.
Journal ArticleDOI
The cristae modulator Optic atrophy 1 requires mitochondrial ATP synthase oligomers to safeguard mitochondrial function.
Ruben Quintana-Cabrera,Charlotte Quirin,Christina Glytsou,Christina Glytsou,Mauro Corrado,Mauro Corrado,Andrea Urbani,Anna Pellattiero,Enrique Calvo,Jesús Vázquez,José Antonio Enríquez,José Antonio Enríquez,Christoph Gerle,Maria Eugenia Soriano,Paolo Bernardi,Luca Scorrano +15 more
TL;DR: The authors show that the mitochondrial fusion protein OPA1 protects mitochondria from dysfunction by promoting ATP synthase oligomerization and reversal activity.
References
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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Michael C. Wei,Michael C. Wei,Wei-Xing Zong,Emily H. Cheng,Tullia Lindsten,Vily Panoutsakopoulou,Andrea J. Ross,Kevin A. Roth,Grant R. MacGregor,Craig B. Thompson,Stanley J. Korsmeyer +10 more
TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
Journal ArticleDOI
The Pathophysiology of Mitochondrial Cell Death
Douglas R. Green,Guido Kroemer +1 more
TL;DR: The therapeutic induction of MOMP may restore apoptosis in cancer cells in which it is disabled, and the general rules governing the pathophysiology and controversial issues regarding its regulation are discussed.
Journal ArticleDOI
Two CD95 (APO-1/Fas) signaling pathways
Carsten Scaffidi,Simone Fulda,Anu Srinivasan,Claudia Friesen,Feng Li,Kevin J. Tomaselli,Klaus-Michael Debatin,Peter H. Krammer,Marcus E. Peter +8 more
TL;DR: In the presence of caspase‐3 the amount of active casp enzyme‐8 generated at the DISC determines whether a mitochondria‐independent apoptosis pathway is used (type I cells) or not (type II cells).
Journal Article
The expanding role of mitochondria in apoptosis
TL;DR: The complexity of the apoptotic program began to increase with the discovery of Bcl-2, a gene whose product causes resistance to apoptosis in lymphocytes, and the complex role of mitochondria in apoptosis came into focus when biochemical studies identified several mitochondrial proteins that are able to activate cellular apoptotic programs directly.
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Mitofusins Mfn1 and Mfn2 coordinately regulate mitochondrial fusion and are essential for embryonic development
TL;DR: It is concluded that Mfn1 and Mfn2 have both redundant and distinct functions and act in three separate molecular complexes to promote mitochondrial fusion, and by enabling cooperation between mitochondria, has protective effects on the mitochondrial population.