Endoplasmic Reticulum Stress: An Opportunity for Neuroprotective Strategies After Stroke

Abstract

Worldwide, ischaemic stroke is a major cause of death and the leading cause of acquired disability. To date, pharmacological thrombolysis with tissue-type plasminogen activator (alone or with mechanical thrombectomy) remains the gold standard acute treatment for ischaemic stroke. Many strategies of neuroprotection have been tested in the past, but none has ever succeeded in clinical trials. Accumulating evidence suggests that stroke activates the endoplasmic reticulum (ER) stress response, which likely deleteriously contribute to stroke damages. However, this remains to be clearly established. In the present chapter, we provide a snapshot on ER stress in ischaemic stroke, and intend to show that knowledge on ER stress in ischaemic context affecting other organs than the brain can provide interesting therapeutic avenues for neuroprotection.