http://www.biomedcentral.com/content/pdf/1471-2202-14-46.pdf
Background
Ischemic stroke is a major cause of neurological disability and a big burden on the family and society. Regaining function can significantly reduce dependence and improve the quality of life of stroke survivors. Ischemic stroke has a very complex pathophysiology. In addition to irreversible neuronal damage, ischemia also triggers cellular processes for neuronal repairinvolving remaining neurons. Apoptosis and necrosis are two vital types of cell death in ischemic brain injury [1]. Recently, autophagic cell death has been reported as a third type of cell death in ischemic tissue [2,3]. Autophagy is a lysosomal pathway for recycling of organelles and long-lived proteins [4,5]. In the course of autophagy, autophagosomes or autophagic vacuoles, are formed to sequester cytoplasmic constituents
[6]. The autophagosomes fuse with lysosomes to digest the contents for recycling. Physiologically, autophagy plays a key role in adapting to nutritional deprivation and eliminating aggregated proteins [7]. However, inappropriate activation of autophagy may lead to cell death in cerebral ischemia [2,3,8,9]. Although it is unclear whether autophagy prevents or contributes to apoptotic cell death, the interaction between autophagy-related and apoptosis-related proteins, suggests an interplay between apoptosis and autophagy [10,11]. On the other hand, stroke also induces neurogenesis [12,13]. It has been reported that newborn neurons can contribute to functional recovery after stroke [1,12]. Interestingly, down-regulation of either autophagy or apoptosis can increase neurogenesis after stroke [1]. Therefore, the functional outcome may be resulted from a complex interplay among autophagy, apoptosis and neurogenesis following cerebral ischemia.
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