When MFN2 (mitofusin 2) met autophagy: A new age for old muscles

A long-standing quest is to define the mechanisms responsible for the mitochondrial dysfunction and accumulation of damaged mitochondria that occur during aging. Indeed, those defects are considered major contributors to the aging process. We have analyzed the effect of aging on the muscle expressio...

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Bibliographic Details
Published inAutophagy Vol. 12; no. 11; pp. 2250 - 2251
Main Authors Sebastián, David, Zorzano, Antonio
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 01.11.2016
Subjects
aging
Aging - pathology
Animals
Autophagic Punctum
Autophagy
Humans
Mice
mitochondria
Mitochondrial Proteins - metabolism
mitophagy
Models, Biological
muscle
Muscles - metabolism
Muscles - pathology
sarcopenia
mitophagy
aging
mitochondria
muscle
sarcopenia
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Summary:A long-standing quest is to define the mechanisms responsible for the mitochondrial dysfunction and accumulation of damaged mitochondria that occur during aging. Indeed, those defects are considered major contributors to the aging process. We have analyzed the effect of aging on the muscle expression of Mfn2 and the impact of Mfn2 ablation on muscle function. Our findings reveal that Mfn2 is repressed in muscle during aging, and that is a determinant for the inhibition of autophagy, and mitochondrial quality control, which lead to the accumulation of damaged mitochondria.
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Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/kaup.
ISSN:1554-8627
1554-8635
DOI:10.1080/15548627.2016.1215383