Cell death is a major determinant of inflammatory disease severity. Whether cells live or die during inflammation largely depends on the relative success of the pro-survival process of autophagy versus the pro-death process of apoptosis. These processes interact and influence each other during inflammation and there is a checkpoint at which cells irrevocably commit to either one pathway or another. This review will discuss the concept of the autophagy/apoptosis checkpoint and its importance during inflammation, the mechanisms of inflammation leading up to the checkpoint, and how the checkpoint is regulated. Understanding these concepts is important since manipulation of the autophagy/apoptosis checkpoint represents a novel opportunity for treatment of inflammatory diseases caused by too much or too little cell death.
Keywords: Atg5; Beclin-1; Calpain; Caspase; HMGB1.