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Molecular mechanisms of aging-associated inflammation.

Abstract
A direct relationship exists between aging and increasing incidences of chronic diseases. In fact, with most age-associated diseases individuals manifest an underlying chronic inflammatory state as evidenced by local infiltration of inflammatory cells, such as macrophages, and higher circulatory levels of pro-inflammatory cytokines, complement components and adhesion molecules. Consequently, treatment with anti-inflammatory agents provide symptomatic relief to several aging-associated diseases, even as remote as Alzheimer's or Parkinson's disease, indicating that chronic inflammation may play a substantial role in the pathogenesis of these disease states. The molecular mechanisms underlying this chronic inflammatory condition during cellular senescence is presently unclear. Cellular damage by oxygen free radicals is a primary driving force for aging and increased activation of redox-regulated transcription factors, such as NF-kappaB that regulate the expression of pro-inflammatory molecules, has been documented in aged animals/individuals versus their young counterparts. Human polynucleotide phosphorylase (hPNPase(old-35)), a RNA degradation enzyme shown to be upregulated during differentiation and cellular senescence, may represent a molecular link between aging and its associated inflammation. hPNPase(old-35) promotes reactive oxygen species (ROS) production, activates the NF-kappaB pathway and initiates the production of pro-inflammatory cytokines, such as IL-6 and IL-8. In these contexts, inhibition of hPNPase(old-35) may represent a novel molecular target for intervening in aging-associated chronic diseases.
AuthorsDevanand Sarkar, Paul B Fisher
JournalCancer letters (Cancer Lett) Vol. 236 Issue 1 Pg. 13-23 (May 08 2006) ISSN: 0304-3835 [Print] Ireland
PMID15978720 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Anti-Inflammatory Agents
  • Chemokines
  • Cytokines
  • Enzyme Inhibitors
  • Free Radicals
  • NF-kappa B
  • Reactive Oxygen Species
  • Exoribonucleases
  • PNPT1 protein, human
  • Acetylcysteine
Topics
  • Acetylcysteine (pharmacology)
  • Aging (metabolism)
  • Animals
  • Anti-Inflammatory Agents (pharmacology)
  • Cell Line, Tumor
  • Cellular Senescence
  • Chemokines (metabolism)
  • Cytokines (metabolism)
  • Enzyme Inhibitors (pharmacology)
  • Exoribonucleases (antagonists & inhibitors, genetics, metabolism)
  • Free Radicals (chemistry, metabolism)
  • Humans
  • Inflammation (drug therapy, etiology, metabolism)
  • NF-kappa B (genetics, metabolism)
  • Neurodegenerative Diseases (drug therapy, etiology, metabolism)
  • Reactive Oxygen Species (metabolism)

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