Time-Dependent Changes in Apoptosis Upon Autophagy Inhibition in Astrocytes Exposed to Oxygen and Glucose Deprivation.

Recent studies have implicated the role of autophagy in brain ischemia pathophysiology. However, it remains unclear whether autophagy activation is protective or detrimental to astrocytes undergoing ischemic stress. This study evaluated the influence of ischemia-induced autophagy on cell death and the course of intrinsic and extrinsic apoptosis in primary cultures of rat cortical astrocytes exposed to combined oxygen-glucose deprivation (OGD).

[Astrocytes in ischemic stroke - a potential target for neuroprotective strategies].

Ischemic stroke is one of the leading causes of adult death and disability worldwide. Present applied therapeutic strategies do not give satisfactory results. It is often emphasized that pharmacological actions aimed at reducing the area of ischemic brain injury should protect astrocytes forming together with neurons and the endothelium neurovascular unit.

AMP-activated protein kinase is involved in induction of protective autophagy in astrocytes exposed to oxygen-glucose deprivation.

AMP-activated kinase (AMPK) acts as the intracellular ATP depletion sensor, which detects and limits increases in the AMP/ATP ratio. AMPK may be significantly activated under stress conditions that deplete cellular ATP levels such as ischemia/hypoxia or glucose deprivation. Recent studies strongly suggest that AMPK participates in autophagy regulation, but it is not known whether AMPK activated by ischemia regulates autophagy in astrocytes and the consequence of autophagy activation in ischemic astrocytes are unclear.

Neuronal autophagy in cerebral ischemia--a potential target for neuroprotective strategies?

Although many attempts have been made, stroke treatment options are still extremely limited and brain ischemia remains the leading cause of death and disability worldwide. Two major strategies for ischemic stroke, reperfusion and neuroprotection, are currently being evaluated. Autophagy is a bulk protein degradation system that is involved in multiple cellular processes.

[Autophagy in brain ischemia].

Autophagy is an intracellular process of macromolecule and organelle degradation, which plays an important role both in maintaining homeostasis and in responding to various harmful stimuli. Recent studies clearly indicate upregulation of autophagy in neurons challenged with brain ischemia. In this paper we present biosynthesis of autophagosomes as well as the role and molecular mechanisms of basal and induced neuronal autophagy.