کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1930046 | 1050488 | 2012 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Oxidative stress induces mitochondrial fragmentation in frataxin-deficient cells Oxidative stress induces mitochondrial fragmentation in frataxin-deficient cells](/preview/png/1930046.png)
Friedreich ataxia (FA) is the most common recessive neurodegenerative disease. It is caused by deficiency in mitochondrial frataxin, which participates in iron–sulfur cluster assembly. Yeast cells lacking frataxin (Δyfh1 mutant) showed an increased proportion of fragmented mitochondria compared to wild-type. In addition, oxidative stress induced complete fragmentation of mitochondria in Δyfh1 cells. Genetically controlled inhibition of mitochondrial fission in these cells led to increased resistance to oxidative stress. Here we present evidence that in yeast frataxin-deficiency interferes with mitochondrial dynamics, which might therefore be relevant for the pathophysiology of FA.
► Yeast frataxin-deficiency leads to increased proportion of fragmented mitochondria.
► Oxidative stress induces complete mitochondrial fragmentation in Δyfh1 cells.
► Oxidative stress increases mitochondrial fragmentation in patient fibroblasts.
► Inhibition of mitochondrial fission in Δyfh1 induces oxidative stress resistance.
Journal: Biochemical and Biophysical Research Communications - Volume 418, Issue 2, 10 February 2012, Pages 336–341