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
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Optic Atrophy 1-Dependent Mitochondrial Remodeling Controls Steroidogenesis in Trophoblasts
Michał Wasilewski,Martina Semenzato,Susanne M. Rafelski,Jennifer R. Robbins,Anna I. Bakardjiev,Luca Scorrano +5 more
TL;DR: It is shown that the mitochondria-shaping protein Optic atrophy 1 (Opa1) controls efficiency of steroidogenesis, and accumulation of cholesterol is facilitated in the inner membrane of isolated mitochondria lacking Opa1.
Journal ArticleDOI
Mitochondria-targeted therapies for acute kidney injury.
Luis Carlos Tábara,Jonay Poveda,Catalina Martin-Cleary,Rafael Selgas,Alberto Ortiz,Maria Dolores Sanchez-Niño +5 more
TL;DR: The morphological and functional mitochondrial changes during AKI are reviewed, as well as changes in the expression of mitochondrial genes and proteins, and the current status of novel therapeutic strategies specifically targeting mitochondria are summarized.
Journal ArticleDOI
Mitochondrial-Shaping Proteins in Cardiac Health and Disease – the Long and the Short of It!
Sang Bing Ong,Siavash Beikoghli Kalkhoran,Sauri Hernández-Reséndiz,Sauri Hernández-Reséndiz,Parisa Samangouei,Sang-Ging Ong,Derek J. Hausenloy +6 more
TL;DR: Interestingly, in the adult heart, it appears that the pleiotropic effects of the mitochondrial fusion proteins, Mfn2 and OPA1 may play more important roles than their pro-fusion effects.
Journal ArticleDOI
Targeting mitochondrial dysfunction in neurodegenerative disease: Part II.
Victoria S Burchell,Sonia Gandhi,Emma Deas,Nicholas W. Wood,Andrey Y. Abramov,Helene Plun-Favreau +5 more
TL;DR: This review examines the role of mitochondrial dysfunction in neurodegeneration, drawing examples from common diseases such as Alzheimer's disease and rarer familial disorders such as Charcot-Marie-Tooth.
Journal ArticleDOI
Organellar vs cellular control of mitochondrial dynamics
TL;DR: The different global and local signals that control mitochondrial biology are investigated to clarify the different signals that impact the status of the mitochondrial population.
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.