2013
DOI: 10.1111/acel.12118
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Summary Aging and age-related pathology is a result of a still incompletely-understood intricate web of molecular and cellular processes. We present a C57BL/6J female mice in vivo aging study of five organs (liver, kidney, spleen, lung and brain), in which we compare genome-wide gene expression profiles during chronological aging with pathological changes throughout the entire murine lifespan (13, 26, 52, 78, 104 and 130 weeks). Relating gene expression changes to chronological aging revealed many differential… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
4
1

Citation Types

3
60
1

Year Published

2014
2014
2023
2023

Publication Types

Select...
9
1

Relationship

0
10

Authors

Journals

citations
Cited by 59 publications
(64 citation statements)
references
References 43 publications
3
60
1
Order By: Relevance
“…Note that testicular development is mostly completed at the start of DR. * p<0.05, ** p<0.01, ***p<0.001. As for wt controls the values do not change significantly in the timeframes used here (see 40 ). Pathological scores, including those of other liver and kidney aging-related histopathological phenotypes are given in Supplementary Table 1.…”
Section: Extended Datamentioning
confidence: 67%
“…Note that testicular development is mostly completed at the start of DR. * p<0.05, ** p<0.01, ***p<0.001. As for wt controls the values do not change significantly in the timeframes used here (see 40 ). Pathological scores, including those of other liver and kidney aging-related histopathological phenotypes are given in Supplementary Table 1.…”
Section: Extended Datamentioning
confidence: 67%
“…Large scale age-related gene expression studies showed that the changes in immune responses with aging are closely related to gene expression in multiple organs. For example, decreases in the expression of immune-related genes in spleen were suggested to be responsible for the decrease in immune responses in aging (36, 38, 39). Our current study reveals a new causal role for deficits in transcriptional expression of Rac1 in diminished AMϕ phagocytosis of E. coli in aging.…”
Section: Discussionmentioning
confidence: 99%
“…Aging is linked to disrupted protein homeostasis and accumulation of misfolded proteins (David et al ., 2010) that is also a unifying mechanism of progressive neurodegenerative diseases (Ross & Poirier, 2004). In parallel, accumulation of lysosomal aggregates (lipofuscin) is a well-characterized histopathological hallmark of neuronal aging (Jonker et al ., 2013; Terzibasi Tozzini et al ., 2013). Finally, down-regulation of proteasome is observed both in N. furzeri and human (Table1), and the network of coregulated genes at the oldest age shows enrichment for ER stress response and protein folding (Fig.…”
Section: Discussionmentioning
confidence: 99%