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Updated: Feb 9, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
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Published on: August 18, 2015

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Danger signals in stroke and their role on microglia activation after ischemia

Eileen Gülke1, Mathias Gelderblom2, Tim Magnus2

  • 1Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Therapeutic Advances in Neurological Disorders
|June 2, 2018
PubMed

Insights

Ischemic stroke causes cell death partly through sterile inflammation. Damage-associated molecular patterns (DAMPs) released from dying cells activate immune responses, exacerbating stroke damage.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Ischemic stroke is a leading cause of mortality.
  • Beyond direct cell damage from oxygen/glucose deprivation, sterile inflammation significantly contributes to cell death.
  • Damage-associated molecular patterns (DAMPs) are key mediators of this inflammatory response.

Purpose of the Study:

  • To review the critical role of DAMPs in ischemic stroke.
  • To elucidate the specific DAMPs involved and their mechanisms.
  • To detail the intracellular pathways DAMPs activate in microglia.

Main Methods:

  • Literature review focusing on DAMPs in ischemic stroke.
  • Analysis of DAMPs including HMGB1, heat/cold shock proteins, purines, and peroxiredoxins.
  • Examination of DAMP-mediated intracellular signaling in microglia.

Main Results:

  • DAMPs are passively released from necrotic cells post-stroke.
  • These DAMPs rapidly activate the innate immune system, driving inflammation.
  • Key DAMPs like HMGB1, HSPs, purines, and peroxiredoxins are implicated.

Conclusions:

  • DAMPs are crucial drivers of sterile inflammation and secondary cell death in ischemic stroke.
  • Understanding DAMPs and their microglial pathways offers therapeutic targets.
  • Targeting DAMPs may mitigate stroke-induced brain damage.
Keywords:
DAMPsHMGB1Hspmicrogliaperoxiredoxinpurinesstroke

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