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Inflammatory networks during cellular senescence: causes and consequences

Journal

TRENDS IN MOLECULAR MEDICINE
Volume 16, Issue 5, Pages 238-246

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2010.03.003

Keywords

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Funding

  1. US National Institutes of Health research [AG09909, AG025901, AG017242]
  2. US National Institutes of Health research center [AG025708, AG032117]
  3. Larry L. Hillblom Foundation
  4. National Science Foundation
  5. NATIONAL INSTITUTE ON AGING [R01AG009909, P30AG025708, R56AG009909, R37AG009909, T32AG000266, P01AG025901, RL1AG032117, P01AG017242] Funding Source: NIH RePORTER

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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.

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