Inflammatory networks during cellular senescence: causes and consequences

被引:1018
作者
Freund, Adam [1 ,2 ]
Orjalo, Arturo V. [1 ]
Desprez, Pierre-Yves [1 ,3 ]
Campisi, Judith [1 ,4 ]
机构
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[3] Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA
[4] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA
基金
美国国家卫生研究院; 美国国家科学基金会;
关键词
ONCOGENE-INDUCED SENESCENCE; NF-KAPPA-B; BENIGN PROSTATIC HYPERPLASIA; TUMOR SUPPRESSION; HUMAN FIBROBLASTS; STEM-CELLS; IN-VIVO; CARDIOVASCULAR-DISEASE; SECRETORY PHENOTYPE; CHROMATIN-STRUCTURE;
D O I
10.1016/j.molmed.2010.03.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic inflammation is associated with aging and plays a causative role in several age-related diseases such as cancer, atherosclerosis and osteoarthritis. The source of this chronic inflammation is often attributed to the progressive activation of immune cells over time. However, recent studies have shown that the process of cellular senescence, a tumor suppressive stress response that is also associated with aging, entails a striking increase in the secretion of proinflammatory proteins and might be an important additional contributor to chronic inflammation. Here, we list the secreted factors that make up the proinflammatory phenotype of senescent cells and describe the impact of these factors on tissue homeostasis. We also summarize the cellular pathways/processes that are known to regulate this phenotype - namely, the DNA damage response, micro-RNAs, key transcription factors and kinases and chromatin remodeling.
引用
收藏
页码:238 / 246
页数:9
相关论文
共 77 条
[1]   Chemokine signaling via the CXCR2 receptor reinforces senescence [J].
Acosta, Juan C. ;
O'Loghlen, Ana ;
Banito, Ana ;
Guijarro, Maria V. ;
Augert, Arnaud ;
Raguz, Selina ;
Fumagalli, Marzia ;
Da Costa, Marco ;
Brown, Celia ;
Popov, Nikolay ;
Takatsu, Yoshihiro ;
Melamed, Jonathan ;
di Fagagna, Fabrizio d'Adda ;
Bernard, David ;
Hernando, Eva ;
Gil, Jesus .
CELL, 2008, 133 (06) :1006-1018
[2]   Remodeling of chromatin structure in senescent cells and its potential impact on tumor suppression and aging [J].
Adams, Peter D. .
GENE, 2007, 397 (1-2) :84-93
[3]   Remodeling chromatin for senescence [J].
Adams, Peter D. .
AGING CELL, 2007, 6 (04) :425-427
[4]   The gene expression program of prostate fibroblast senescence modulates neoplastic epithelial cell proliferation through paracrine mechanisms [J].
Bavik, C ;
Coleman, I ;
Dean, JP ;
Knudsen, B ;
Plymate, S ;
Nelson, PS .
CANCER RESEARCH, 2006, 66 (02) :794-802
[5]   The signals and pathways activating cellular senescence [J].
Ben-Porath, I ;
Weinberg, RA .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2005, 37 (05) :961-976
[6]   MicroRNAs miR-146a/b negatively modulate the senescence associated inflammatory mediators IL-6 and IL-8 [J].
Bhaumik, Dipa ;
Scott, Gary K. ;
Schokrpur, Shiruyeh ;
Patil, Christopher K. ;
Orjalo, Arturo V. ;
Rodier, Francis ;
Lithgow, Gordon J. ;
Campisi, Judith .
AGING-US, 2009, 1 (04) :402-411
[7]   Oncogene-induced senescence as an initial barrier in lymphoma development [J].
Braig, M ;
Lee, S ;
Loddenkemper, C ;
Rudolph, C ;
Peters, AHFM ;
Schlegelberger, B ;
Stein, H ;
Dörken, B ;
Jenuwein, T ;
Schmitt, CA .
NATURE, 2005, 436 (7051) :660-665
[8]   Oncogene-induced senescence: Putting the brakes on tumor development [J].
Braig, M ;
Schmitt, CA .
CANCER RESEARCH, 2006, 66 (06) :2881-2884
[9]   CYTOKINE EXPRESSION IN CHRONIC INFLAMMATORY DISEASE [J].
BRENNAN, FM ;
MAINI, RN ;
FELDMANN, M .
BRITISH MEDICAL BULLETIN, 1995, 51 (02) :368-384
[10]   Unregulated inflammation shortens human functional longevity [J].
Brod, SA .
INFLAMMATION RESEARCH, 2000, 49 (11) :561-570