Autophagy is a lysosome-mediated catabolic process involving the degradation of 
intracellular contents (e.g., proteins and organelles) as well as invading 
microbes (e.g., parasites, bacteria and viruses). Multiple forms of cellular 
stress can stimulate this pathway, including nutritional imbalances, oxygen 
deprivation, immunological response, genetic defects, chromosomal anomalies and 
cytotoxic stress. Damage-associated molecular pattern molecules (DAMPs) are 
released by stressed cells undergoing autophagy or injury, and act as endogenous 
danger signals to regulate the subsequent inflammatory and immune response. A 
complex relationship exists between DAMPs and autophagy in cellular adaption to 
injury and unscheduled cell death. Since both autophagy and DAMPs are important 
for pathogenesis of human disease, it is crucial to understand how they 
interplay to sustain homeostasis in stressful or dangerous environments.