Mitochondria, Oxidative Stress and Innate Immunity

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Mitochondria, Oxidative Stress and Innate Immunity

DOI: 10.3389/fphys.2018.01487

Canonical functions of mitochondria include the regulation of cellular survival, orchestration of anabolic and metabolic pathways, as well as reactive oxygen species (ROS) signaling. Recent discoveries, nevertheless, have demonstrated that mitochondria are also critical elements to stimulate innate immune signaling cascade that is able to intensify the inflammation upon cytotoxic stimuli beyond microbial infection.

Mitochondria are not only house machineries that support cellular essential activities, but also important sources of endogenous DAMPs including ROS as well as necessary triggers for inflammasome signaling. A large number of evidence has emerged linking dysfunctional mitochondria to aberrant innate immune responses. Nevertheless, our understanding of precise roles the inflammasomes in response to mitochondrial malfunction and ROS are still lacking. Many significant questions regarding the molecular machineries which initiate inflammasome activation upon mitochondria disorder and ROS remain to be addressed. Further elucidation of the interplay of ROS, mitochondrial function and inflammasome pathways might open up a new horizon for the development of immunotherapeutic strategy for chronic inflammation diseases such as cardiovascular diseases.