Inflammatory networks during cellular senescence: causes and consequences.
Inflammatory networks during cellular senescence: causes and consequences.
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DOI：
10.1016/j.molmed.2010.03.003
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发表时间：
2010-05
影响因子：
13.6
通讯作者：
Campisi J
中科院分区：
文献类型：
--
作者：
Freund A;Orjalo AV;Desprez PY;Campisi J
慢性炎症与衰老有关，在癌症、动脉粥样硬化和骨关节炎等几种与年龄有关的疾病中起着致病作用。这种慢性炎症的来源通常归因于免疫细胞随着时间的推移逐渐激活。然而，最近的研究表明，细胞衰老的过程，也与衰老相关的肿瘤抑制应激反应，需要促炎蛋白分泌的显着增加，可能是慢性炎症的重要额外贡献者。在这里，我们列出了分泌的因素，使促炎表型的衰老细胞，并描述了这些因素对组织稳态的影响。我们还总结了已知调节这种表型的细胞途径/过程-即DNA损伤反应，microRNA，关键转录因子和激酶以及染色质重塑。
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 pro-inflammatory proteins and might be an important additional contributor to chronic inflammation. Here, we list the secreted factors that make up the pro-inflammatory 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, microRNAs, key transcription factors and kinases and chromatin remodeling.
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影响因子：
78.5
作者：
Collado, Manuel;Serrano, Manuel
通讯作者：
Serrano, Manuel
影响因子：
3.7
作者：
Coppé JP;Patil CK;Rodier F;Krtolica A;Beauséjour CM;Parrinello S;Hodgson JG;Chin K;Desprez PY;Campisi J
通讯作者：
Campisi J
影响因子：
11.2
作者：
Bavik, C;Coleman, I;Nelson, PS
通讯作者：
Nelson, PS
DOI：
10.1073/pnas.92.20.9363
发表时间：
1995-09-26
影响因子：
11.1
作者：
DIMRI, GP;LEE, XH;CAMPISI, J
通讯作者：
CAMPISI, J
DOI：
10.1146/annurev-pathol-121808-102144
发表时间：
2010
期刊：
Annual review of pathology
影响因子：
--
作者：
Coppé JP;Desprez PY;Krtolica A;Campisi J
通讯作者：
Campisi J