Abstract
Macroautophagy or autophagy is an evolutionarily well-conserved cellular mechanism by which the cellular contents are engulfed by autophagosomes and delivered to lysosomes for degradation. At present, the involvement of autophagy in cell death remains a highly controversial and debatable topic. On the one hand, it has been well established that autophagy is an important mechanism protecting cells under stress such as starvation via provision of nutrients and removal of protein aggregates and damaged mitochondria. On the other hand, there is accumulating evidence suggesting pro-death function of autophagy, either via promotion of apoptosis or autophagic cell death. At present, the molecular cross talk between autophagy and apoptosis have been well discussed, while the relationship between autophagy and various forms of programmed necrotic cell death is less understood. In this chapter we focus on the role of autophagy in necrotic cell death. We first present the evidence showing the anti-necrosis function of autophagy, and then discuss the biological significance of the anti-necrosis function of autophagy in cancer and ischemia–reperfusion injury. Taken together, we believe that one important aspect of the pro-survival function of autophagy is achieved via its ability to block various forms of necrotic cell death.
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Acknowledgements
The authors would like to thank Kaihui Lu for the contribution in preparing the manuscript and Youtong Wu for preparation of Fig. 13.1. Work in HMS’s laboratory is supported by research grants from Singapore National Medical Research Council (NMRC/1260/2010) and Singapore Biomedical Research Council (BMRC/08/1/21/19/554). Work in PC laboratory is supported by funding from INSERM and grants from ANR and INCa.
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Shen, HM., Codogno, P. (2014). Autophagy in Necrosis: A Force for Survival. In: Shen, HM., Vandenabeele, P. (eds) Necrotic Cell Death. Cell Death in Biology and Diseases. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4614-8220-8_13
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DOI: https://doi.org/10.1007/978-1-4614-8220-8_13
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