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Mitochondrial fusion, fission and autophagy as a quality control axis: The bioenergetic view

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TLDR
Pairs of fusion and fission allow for the reorganization and sequestration of damaged mitochondrial components into daughter mitochondria that are segregated from the networking pool and then becoming eliminated by autophagy.
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This article is published in Biochimica et Biophysica Acta.The article was published on 2008-05-14 and is currently open access. It has received 593 citations till now. The article focuses on the topics: Mitochondrial fission & mitochondrial fusion.

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Mitochondrial dynamics in the regulation of nutrient utilization and energy expenditure.

TL;DR: Placement of bioenergetic adaptation and quality control as competing tasks of mitochondrial dynamics might provide a new mechanism, linking excess nutrient environment to progressive mitochondrial dysfunction, common to age-related diseases.
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Mitochondria in Neuroplasticity and Neurological Disorders

TL;DR: Mitochondrial electron transport generates the ATP that is essential for the excitability and survival of neurons, and the protein phosphorylation reactions that mediate synaptic signaling and related long-term changes in neuronal structure and function.
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Mitochondria-Anchored Receptor Atg32 Mediates Degradation of Mitochondria via Selective Autophagy

TL;DR: It is demonstrated that, in post-log phase cells under respiratory conditions, a substantial fraction of mitochondria are exclusively sequestered as cargoes and transported to the vacuole, a lytic compartment in yeast, in an autophagy-dependent manner and suggested that Atg32, a mitochondria-anchored protein essential for mitophagy that is induced during respiratory growth, interacts with Atg8 and Atg11, autophatic proteins critical for recognition of cargo receptors.
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Mitochondrial dysfunction and oxidative stress in metabolic disorders — A step towards mitochondria based therapeutic strategies

TL;DR: The purpose of the article is to highlight the recent progress on the mitochondrial role in metabolic syndromes and also summarize the progress of mitochondria-targeted molecules as therapeutic targets to treat metabolic Syndromes.
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Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin

TL;DR: It is shown in Drosophila cells that PINK1 is required to recruit Parkin to dysfunctional mitochondria and promote their degradation, and Mfn ubiquitination may provide a mechanism by which terminally damaged mitochondria are labeled and sequestered for degradation by autophagy.
References
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Journal ArticleDOI

Imaging intracellular fluorescent proteins at nanometer resolution.

TL;DR: This work introduced a method for optically imaging intracellular proteins at nanometer spatial resolution and used this method to image specific target proteins in thin sections of lysosomes and mitochondria and in fixed whole cells to image retroviral protein Gag at the plasma membrane.
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Mitochondrial Membrane Permeabilization in Cell Death

TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
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Self-eating and self-killing: crosstalk between autophagy and apoptosis

TL;DR: The functional relationship between apoptosis and autophagy is complex in the sense that, under certain circumstances,autophagy constitutes a stress adaptation that avoids cell death (and suppresses apoptosis), whereas in other cellular settings, it constitutes an alternative cell-death pathway.
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Autophagy: from phenomenology to molecular understanding in less than a decade

TL;DR: In 2000, it was suggested to me that “Autophagy will be the wave of the future; it will become the new apoptosis,” and this statement turned out to be prophetic, and this process of 'self-eating' rapidly exploded as a research field, as scientists discovered connections to cancer, neurodegeneration and even lifespan extension.
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