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

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

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

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

scholarly journals MITOL deletion in the brain impairs mitochondrial structure and ER tethering leading to oxidative stress

2019 ◽  
Vol 2 (4) ◽  
pp. e201900308 ◽  
Author(s):  
Shun Nagashima ◽  
Keisuke Takeda ◽  
Nobuhiko Ohno ◽  
Satoshi Ishido ◽  
Motohide Aoki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Microglial Activation ◽  
Developmental Disorders ◽  
Inflammatory Diseases ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Three Dimensional ◽  
Abnormal Behavior ◽  
Mitochondrial Abnormalities

Mitochondrial abnormalities are associated with developmental disorders, although a causal relationship remains largely unknown. Here, we report that increased oxidative stress in neurons by deletion of mitochondrial ubiquitin ligase MITOL causes a potential neuroinflammation including aberrant astrogliosis and microglial activation, indicating that mitochondrial abnormalities might confer a risk for inflammatory diseases in brain such as psychiatric disorders. A role of MITOL in both mitochondrial dynamics and ER-mitochondria tethering prompted us to characterize three-dimensional structures of mitochondria in vivo. In MITOL-deficient neurons, we observed a significant reduction in the ER-mitochondria contact sites, which might lead to perturbation of phospholipids transfer, consequently reduce cardiolipin biogenesis. We also found that branched large mitochondria disappeared by deletion of MITOL. These morphological abnormalities of mitochondria resulted in enhanced oxidative stress in brain, which led to astrogliosis and microglial activation partly causing abnormal behavior. In conclusion, the reduced ER-mitochondria tethering and excessive mitochondrial fission may trigger neuroinflammation through oxidative stress.

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