Advances in the understanding of mitochondrial DNA as a pathogenic factor in inflammatory diseases [version 1; referees: 3 approved]

• Main Authors: Ray K. Boyapati, Arina Tamborska, David A. Dorward, Gwo-Tzer Ho
• Format: Article
• Language: English
• Published: F1000 Research Ltd 2017-02-01
• Series: F1000Research
• Subjects: Acute Cardiovascular Problems; Acute Renal Failure; Autoimmunity; Bleeding & Coagulation Disorders; Cell Signaling; Cellular Death & Stress Responses; Cellular Microbiology & Pathogenesis; Clinical Immunology; Coronary Artery Disease; Diabetes & Obesity; Emergency Medicine; Etiology, Pathogenesis & Animal Models of Rheumatic Disease; Genetics of the Immune System; Heart Failure; Immune & Inflammatory Rheumatic Diseases (incl. Arthritis); Immune Response; Immunity to Infections; Immunopharmacology & Hematologic Pharmacology; Innate Immunity; Leukocyte Signaling & Gene Expression; Liver Biology & Pathobiology; Medical Microbiology; Membranes & Sorting; Neurobiology of Disease & Regeneration; Nuclear Structure & Function; Pediatric Problems in Critical Care; Sepsis & Multiple Organ Failure in Critical Care; Virology
• Online Access: https://f1000research.com/articles/6-169/v1

Mitochondrial DNA (mtDNA) has many similarities with bacterial DNA because of their shared common ancestry. Increasing evidence demonstrates mtDNA to be a potent danger signal that is recognised by the innate immune system and can directly modulate the inflammatory response. In humans, elevated circulating mtDNA is found in conditions with significant tissue injury such as trauma and sepsis and increasingly in chronic organ-specific and systemic illnesses such as steatohepatitis and systemic lupus erythematosus. In this review, we examine our current understanding of mtDNA-mediated inflammation and how the mechanisms regulating mitochondrial homeostasis and mtDNA release represent exciting and previously under-recognised important factors in many human inflammatory diseases, offering many new translational opportunities.