Danger signals in stroke

Mathias Gelderblom; Christopher G Sobey; Christoph Kleinschnitz; Tim Magnus

doi:10.1016/j.arr.2015.07.004

Danger signals in stroke

Ageing Res Rev. 2015 Nov;24(Pt A):77-82. doi: 10.1016/j.arr.2015.07.004. Epub 2015 Jul 22.

Authors

Mathias Gelderblom¹, Christopher G Sobey², Christoph Kleinschnitz³, Tim Magnus⁴

Affiliations

¹ Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246 Hamburg, Germany. Electronic address: m.gelderblom@uke.de.
² Vascular Biology and Immunopharmacology Group, Department of Pharmacology, Monash University, Clayton, Victoria, Australia; Department of Surgery, Monash Medical Centre, Southern Clinical School, Monash University, Clayton, Victoria, Australia.
³ Department of Neurology, University Clinics Wuerzburg, Josef-Schneider-Straße 11, 97080 Wuerzburg, Germany.
⁴ Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246 Hamburg, Germany. Electronic address: t.magnus@uke.de.

PMID: 26210897
DOI: 10.1016/j.arr.2015.07.004

Abstract

Danger molecules are the first signals released from dying tissue after stroke. These danger signals bind to receptors on immune cells that will result in their activation and the release of inflammatory and neurotoxic mediators, resulting in amplification of the immune response and subsequent enlargement of the damaged brain volume. The release of danger signals is a central event that leads to a multitude of signals and cascades in the affected and neighbouring tissue, therefore providing a potential target for therapy.

Keywords: DAMP; HMGB1; Hsp; Inflammation; Stroke.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Humans
Stroke / immunology
Stroke / metabolism*
Stroke / pathology*