DAMPs as mediators of sterile inflammation in aging-related pathologies

Noa Feldman1, Aviva Rotter-Maskowitz1, Eitan Okun1

  • 1The Mina and Everard Goodman Faculty of Life Sciences, The Gonda Multidisciplinary Brain Research Center, Bar Ilan University, Ramat-Gan 5290002, Israel.

Ageing Research Reviews
|February 3, 2015
PubMed

Insights

Aging involves chronic sterile-inflammation, a pathogen-free inflammatory response. Danger-associated molecular patterns (DAMPs) activate immune receptors like toll-like receptors (TLRs) and NLRP3, driving inflammation in aging and related diseases.

Area of Science:

  • Immunology
  • Aging Research
  • Molecular Biology

Background:

  • Aging is characterized by chronic, low-level inflammation known as sterile-inflammation.
  • Sterile-inflammation is triggered by non-infectious damage signals, including trauma, ischemia, stress, and UV radiation.
  • These stimuli release danger-associated molecular patterns (DAMPs), which activate innate immune pathways.

Purpose of the Study:

  • To review current knowledge on DAMPs-mediated sterile-inflammation.
  • To summarize downstream signaling pathways involved in DAMPs-induced inflammation.
  • To explore the role of DAMPs activating toll-like receptors (TLRs) or the NLRP3 inflammasome in aging and age-related diseases.

Main Methods:

  • Literature review of studies on sterile-inflammation, DAMPs, TLRs, and NLRP3.
  • Analysis of signaling pathways initiated by DAMPs recognition.
  • Synthesis of evidence linking DAMPs-mediated inflammation to the aging process and associated pathologies.

Main Results:

  • DAMPs are endogenous molecules released upon cellular stress or damage.
  • Innate immune receptors, including TLRs and NLRP3, recognize DAMPs.
  • Recognition of DAMPs by these receptors triggers inflammatory signaling cascades.

Conclusions:

  • DAMPs-mediated sterile-inflammation is a key feature of the aging process.
  • TLRs and NLRP3 inflammasome activation by DAMPs are critical mediators of age-related sterile-inflammation.
  • Understanding these pathways may offer therapeutic targets for aging and associated diseases.

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