Background

Autophagy is an intracellular lysosomal degradation pro-autophagic vacuoles [2,3]. However, the mechanism by which ischemia-induced autophagy promotes cell death Xingyong et al. BMC Neuroscience 2013, 14:56 http://www.biomedcentral.com/1471-2202/14/56Bcl-2 family members [6]. Furthermore, Mcl1 also has aUniversity, Guangzhou 510080, PR China Full list of author information is available at the end of the articlecess, which is characterized by the formation of double-membraned autophagosomes. Substantial reports have documented that ischemia-induced autophagy leads to neuronal death following ischemic stroke [1,2]. This autophagy-dependent non-apoptotic cell death is de-fined as autophagic cell death, or type II programmed cell death (PCD), which is characterized by numerous remains unclear. Physiologically, autophagy is tightly modulated by regulators to prevent unbalanced activa-tion. Several regulators, particularly the Bcl-2 family of proteins, also have a critical role in the regulation of apoptosis, suggesting that the integrated regulation of autophagy and apoptosis determines cell fate [4]. The Bcl-2 homologue, myeloid cell leukemia 1 (Mcl1), is an anti-apoptotic member of the Bcl-2 family of proteins. Mcl1 is a mitochondrial protein [5] and is believed to in-hibit cell death through interactions with pro-apoptotic * Correspondence