Mitochondrial abnormalities in the DIDMOAD syndrome

1992 ◽  
Vol 15 (3) ◽  
pp. 315-319 ◽  
Author(s):  
S. Bundey ◽  
K. Poulton ◽  
H. Whitwell ◽  
E. Curtis ◽  
I. A. R. Brown ◽  
...  
Keyword(s):  
Mitochondrial Abnormalities ◽  
Didmoad Syndrome

Mitochondrial Abnormalities in a Streptozotocin-Induced Rat Model of Sporadic Alzheimer's Disease

2013 ◽  
Vol 10 (4) ◽  
pp. 406-419 ◽  
Author(s):  
Sonia C. Correia ◽  
Renato X. Santos ◽  
Maria S. Santos ◽  
Gemma Casadesus ◽  
Joseph C. LaManna ◽  
...  
Keyword(s):  
Rat Model ◽  
Mitochondrial Abnormalities

Protective effects of a mitochondria-targeted small peptide SS31 against hyperglycemia-induced mitochondrial abnormalities in the liver tissues of diabetic mice, Tallyho/JngJ mice

Mitochondrion ◽  
2021 ◽  
Vol 58 ◽  
pp. 49-58 ◽  
Author(s):  
Jasvinder Singh Bhatti ◽  
Kavya Tamarai ◽  
Ramesh Kandimalla ◽  
Maria Manczak ◽  
Xiangling Yin ◽  
...  
Keyword(s):  
Protective Effects ◽  
Diabetic Mice ◽  
Small Peptide ◽  
Mitochondrial Abnormalities ◽  
Liver Tissues

scholarly journals Type I interferons affect the metabolic fitness of CD8+ T cells from patients with systemic lupus erythematosus

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Norzawani Buang ◽  
Lunnathaya Tapeng ◽  
Victor Gray ◽  
Alessandro Sardini ◽  
Chad Whilding ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Lupus Erythematosus ◽  
Type I Interferons ◽  
Type I ◽  
Type I Ifn ◽  
Systemic Lupus ◽  
Mitochondrial Abnormalities

AbstractThe majority of patients with systemic lupus erythematosus (SLE) have high expression of type I IFN-stimulated genes. Mitochondrial abnormalities have also been reported, but the contribution of type I IFN exposure to these changes is unknown. Here, we show downregulation of mitochondria-derived genes and mitochondria-associated metabolic pathways in IFN-High patients from transcriptomic analysis of CD4+ and CD8+ T cells. CD8+ T cells from these patients have enlarged mitochondria and lower spare respiratory capacity associated with increased cell death upon rechallenge with TCR stimulation. These mitochondrial abnormalities can be phenocopied by exposing CD8+ T cells from healthy volunteers to type I IFN and TCR stimulation. Mechanistically these ‘SLE-like’ conditions increase CD8+ T cell NAD+ consumption resulting in impaired mitochondrial respiration and reduced cell viability, both of which can be rectified by NAD+ supplementation. Our data suggest that type I IFN exposure contributes to SLE pathogenesis by promoting CD8+ T cell death via metabolic rewiring.

Mitochondrial abnormalities in oculopharyngeal muscular dystrophy

1996 ◽  
Vol 6 (3) ◽  
pp. 163-166 ◽  
Author(s):  
Kum Thong Wong ◽  
David Dick ◽  
Janice R. Anderson
Keyword(s):  
Muscular Dystrophy ◽  
Oculopharyngeal Muscular Dystrophy ◽  
Mitochondrial Abnormalities

scholarly journals Redox imbalance and mitochondrial abnormalities in the diabetic lung

Redox Biology ◽  
2017 ◽  
Vol 11 ◽  
pp. 51-59 ◽  
Author(s):  
Jinzi Wu ◽  
Zhen Jin ◽  
Liang-Jun Yan
Keyword(s):  
Redox Imbalance ◽  
Mitochondrial Abnormalities

Indomethacin elicits proteasomal dysfunctions develops apoptosis through mitochondrial abnormalities

2017 ◽  
Vol 233 (2) ◽  
pp. 1685-1699 ◽  
Author(s):  
Ayeman Amanullah ◽  
Ribhav Mishra ◽  
Arun Upadhyay ◽  
Pothula P. Reddy ◽  
Ranabir Das ◽  
...  
Keyword(s):  
Mitochondrial Abnormalities
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