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Updated: Feb 3, 2026

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury
Published on: November 19, 2019
Inflammation and neural repair after ischemic brain injury
Seiichiro Sakai1, Takashi Shichita1
1Stroke Renaissance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, 156-8506, Japan.
Abstract:
Stroke causes neuronal cell death and destruction of neuronal circuits in the brain and spinal cord. Injury to the brain tissue induces sterile inflammation triggered by the extracellular release of endogenous molecules, but cerebral inflammation after stroke is gradually resolved within several days. In this pro-resolving process, inflammatory cells adopt a pro-resolving or repairing phenotype in the injured brain, activating endogenous repairing programs. Although the mechanisms involved in the transition from inflammation to neural repair after stroke remain largely unknown to date, some of the mechanisms for inflammation and neural repair have been clarified in detail. This review focuses on the molecular or cellular mechanisms involved in sterile inflammation and neural repair after stroke. This accumulation of evidence may be helpful for speculating about the endogenous repairing mechanisms in the brain and identifying therapeutic targets for improving the functional prognoses of stroke patients.
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