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The Role of Inflammatory Response in Stroke Associated Programmed Cell Death

Journal

CURRENT NEUROPHARMACOLOGY
Volume 16, Issue 9, Pages 1365-1374

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1570159X16666180222155833

Keywords

Inflammation; stroke; necrosis; apoptosis; necroptosis; pyroptosis; autophagy

Funding

  1. Czech Science Foundation (GACR) [14-23773P]

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Stroke represents devastating pathology which is associated with a high morbidity and mortality. Initial damage caused directly by the onset of stroke, primary injury, may be eclipsed by secondary injury which may have a much more devastating effect on the brain. Primary injury is predominantly associated with necrotic cell death due to fatal insufficiency of oxygen and glucose. Secondary injury may on the contrary, lead apoptotic cell death due to structural damage which is not compatible with cellular functions or which may even represent the danger of malign transformation. The immune system is responsible for surveillance, defense and healing processes and the immune system plays a major role in triggering programmed cell death. Severe pathologies, such as stroke, are often associated with deregulation of the immune system, resulting in aggravation of secondary brain injury. The goal of this article is to overview the current knowledge about the role of immune system in the pathophysiology of stroke with respect to programmed neuronal cell death as well as to discuss current therapeutic strategies targeting inflammation after stroke.

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