IAPs are regulated cell-autonomously by several mitochondrial IAP binding motif (IBM)-containing proteins that are released from mitochondria upon disruption of mitochondrial outer membrane (e. g. Smac). Our ongoing studies suggest that mitochondrial respiratory activity not only covers the cellular energy demand but also acts as a molecular relay for cell death and inflammatory signalling. We are specifically investigating how mitochondrial respiratory activity controls the release of factors that interfere with cellular fate and tissue inflammation. Mitochondrial respiratory dysfunction causes aging and aging-associated diseases. It is increasingly evident that distinct mitochondrial alterations also decisively impact on cancer progression and pathogenicity of bacteria. Here we are specifically investigating the impact of this metabolic symbiosis between tumour cells with tumour environment and host-pathogen interaction.