Proteomic Analysis of Exosomes Released from Heatstressed Hepatocytes Reveals Promotion of Programmed Cell Death Pathways

2018 ◽  
Author(s):  
Yue Li ◽  
Xintao Zhu ◽  
Guozhen Wang ◽  
Huasheng Tong ◽  
Xuguang Ling ◽  
...  
2007 ◽  
Vol 14 (5) ◽  
pp. 916-923 ◽  
Author(s):  
D N Martin ◽  
B Balgley ◽  
S Dutta ◽  
J Chen ◽  
P Rudnick ◽  
...  

2002 ◽  
Vol 126 (3) ◽  
pp. 271-280
Author(s):  
Russell H. Swerdlow

Abstract Mitochondrial dysfunction occurs in several late-onset neurodegenerative diseases. Determining its origin and significance may provide insight into the pathogeneses of these disorders. Regarding origin, one hypothesis proposes mitochondrial dysfunction is driven by mitochondrial DNA (mtDNA) aberration. This hypothesis is primarily supported by data from studies of cytoplasmic hybrid (cybrid) cell lines, which facilitate the study of mitochondrial genotype-phenotype relationships. In cybrid cell lines in which mtDNA from persons with certain neurodegenerative diseases is assessed, mitochondrial physiology is altered in ways that are potentially relevant to programmed cell death pathways. Connecting mtDNA-related mitochondrial dysfunction with programmed cell death underscores the crucial if not central role for these organelles in neurodegenerative pathophysiology. This review discusses the cybrid technique and summarizes cybrid data implicating mtDNA-related mitochondrial dysfunction in certain neurodegenerative diseases.


2012 ◽  
Vol 6 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Miao Ming ◽  
Xu Zhao ◽  
Zi-yi Zhao ◽  
Bo Liu ◽  
Jin-ku Bao

2011 ◽  
Vol 39 (5) ◽  
pp. 1520-1526 ◽  
Author(s):  
Ralf J. Braun ◽  
Benedikt Westermann

Mitochondria play crucial roles in programmed cell death and aging. Different stimuli activate distinct mitochondrion-dependent cell death pathways, and aging is associated with a progressive increase in mitochondrial damage, culminating in oxidative stress and cellular dysfunction. Mitochondria are highly dynamic organelles that constantly fuse and divide, forming either interconnected mitochondrial networks or separated fragmented mitochondria. These processes are believed to provide a mitochondrial quality control system and enable an effective adaptation of the mitochondrial compartment to the metabolic needs of the cell. The baker's yeast, Saccharomyces cerevisiae, is an established model for programmed cell death and aging research. The present review summarizes how mitochondrial morphology is altered on induction of cell death or on aging and how this correlates with the induction of different cell death pathways in yeast. We highlight the roles of the components of the mitochondrial fusion and fission machinery that affect and regulate cell death and aging.


2018 ◽  
Vol 221 (2) ◽  
pp. 919-934 ◽  
Author(s):  
Lipu Wang ◽  
Rui Wen ◽  
Jinghe Wang ◽  
Daoquan Xiang ◽  
Qian Wang ◽  
...  

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