Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

0
3
0

Year Published

2016
2016
2021
2021

Publication Types

Select...
3

Relationship

0
3

Authors

Journals

citations
Cited by 3 publications
(3 citation statements)
references
References 17 publications
(21 reference statements)
0
3
0
Order By: Relevance
“…Murakami et al [ 71 ] recently showed that p16(Ink4a) regulates degradation of IRAK1 and consequent secretion of IL-6 in mouse and human macrophages but not fibroblasts. In addition, another senescence-associated tumor suppressor p19ARF has been reported as a new p53-independent regulator of inflammatory response in macrophages modulating TLRs signaling [ 72 , 73 ]. Hence, the induction of the senescence-associated macrophage (SAM) phenotype may not specifically require SCs, but rather represent a specific type of macrophage activation or differentiation in response to certain natural physiological stimuli.…”
Section: Discussionmentioning
confidence: 99%
“…Murakami et al [ 71 ] recently showed that p16(Ink4a) regulates degradation of IRAK1 and consequent secretion of IL-6 in mouse and human macrophages but not fibroblasts. In addition, another senescence-associated tumor suppressor p19ARF has been reported as a new p53-independent regulator of inflammatory response in macrophages modulating TLRs signaling [ 72 , 73 ]. Hence, the induction of the senescence-associated macrophage (SAM) phenotype may not specifically require SCs, but rather represent a specific type of macrophage activation or differentiation in response to certain natural physiological stimuli.…”
Section: Discussionmentioning
confidence: 99%
“…212 ARF is required for MYC to regulate the expression of genes involved in innate immune activation. 100 Interestingly, CD8 + T cells in Cdkn2a –/– mice have been shown to produce significantly lower amounts of IL-10 and thus are more susceptible to 2,4,6-trinitrobenzenesulfonic acid (TNBS)–induced colitis. 216…”
Section: Discussionmentioning
confidence: 99%
“…Chronic wounds and flare-ups are long-term complications after SM exposure and thus there needs to be some kind of “memory”, which may be senescent cells due to their longevity. Senescence is part of many cellular mechanisms including aging (Baker et al 2016 ), age-related diseases (Baker et al 2011 ), tissue remodeling (Krizhanovsky et al 2008 ), wound healing (Jun and Lau 2010 ) and immunity (Kearney et al 2015 ). Recently, senescence was defined as a specific permanent growth arrest of proliferation-competent cell induced by stressors (Sharpless and Sherr 2015 ) like reactive oxygen species (ROS) (von Zglinicki 2002 ) or unresolved DNA damage (Sedelnikova et al 2004 ).…”
Section: Introductionmentioning
confidence: 99%