| Popis: |
Endoplasmic reticulum (ER) stress is a complex cellular mechanism that is induced by the accumulation of misfolded proteins under various stress stimuli. ER stress is implicated in various pathological conditions, including cerebral ischemia. In cerebral ischemia, ER stress is presumed to be an early event and pro-survival. However, its precise involvement in ischemia/reperfusion (IR) injury is still contentious and under investigation. Mechanistically, ER stress and its associated unfolded protein response is presumed to be a defensive mechanism, which, when it becomes chronic, has fatal effects on neuronal survival and outcomes of stroke patients. Recent investigations have presented interesting contributions of autophagy to cerebral ER stress. As an innate process, autophagy is a defensive process for neuronal cell survival, but when triggered by chronic ER stress, it becomes destructive and induces cell death. Moreover, other factors, such as small non-coding microRNAs (miRs), have also been shown to regulate both of these processes through their gene expression regulatory properties. However, it is still very important to understand the interrelationship between ER stress and autophagy in IR injury following cerebral stroke so as to define its therapeutic significance. Furthermore, we need to approach combined therapies using ER stress and autophagy inhibitors with the intent to improve current treatments for cerebral stroke. |
