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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Mechanisms of mitochondrial respiratory adaptation
TL;DR: Mitochondrial adaptive cellular processes are important for physiological responses, including to nutrient availability, temperature and physical activity, and their failure leads to diseases associated with mitochondrial dysfunction such as metabolic and age-associated diseases and cancer.
Journal ArticleDOI
Unacylated ghrelin prevents mitochondrial dysfunction in a model of ischemia/reperfusion liver injury
Alberto Rossetti,Gabriele Togliatto,Anabela P. Rolo,João S. Teodoro,Riccarda Granata,Ezio Ghigo,Amedeo Columbano,Carlos M. Palmeira,Maria Felice Brizzi +8 more
TL;DR: The results demonstrate that UnAG administration rescues the intrinsic mitochondrial pathway triggered by I/R damage and provides the rationale for exploiting UnAG as an alternative means to rescuing mitochondrial damage and organ dysfunction.
Journal ArticleDOI
Membranes in motion: mitochondrial dynamics and their role in apoptosis.
TL;DR: The key components of mitochondrial dynamics have been identified and an interplay between the proteins of the mitochondrial fission/fusion machinery and the Bcl-2 proteins, essential mediators in apoptosis, has been described.
Journal ArticleDOI
Macroautophagy inhibition maintains fragmented mitochondria to foster T cell receptor-dependent apoptosis.
Mauro Corrado,Francesca Romana Mariotti,Laura Trapani,Lucia Taraborrelli,Francesca Nazio,Francesca Nazio,Valentina Cianfanelli,Maria Eugenia Soriano,Emilie Schrepfer,Francesco Cecconi,Luca Scorrano,Silvia Campello +11 more
TL;DR: Autophagy‐forced reactivation that clears the Parkin‐decorated mitochondria is as effective in inhibiting apoptosis as genetic interference with cristae remodelling and cytochrome c release, which ensures apoptotic progression.
Journal ArticleDOI
Loss of Drosophila i-AAA protease, dYME1L, causes abnormal mitochondria and apoptotic degeneration
TL;DR: The results suggest that i-AAA is essential for removing unfolded proteins and maintaining mitochondrial membrane architecture, which might contribute to apoptosis upon the release of proapoptotic molecules such as dOmi.
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.