title: The Roles of Mitochondrial Damage-Associated Molecular Patterns in Diseases.
abstract: CONCLUSIONS
  Mitochondria, vital cellular power plants to generate energy, are involved in immune responses. Mitochondrial damage-associated molecular patterns (DAMPs) are molecules that are released from mitochondria to extracellular space during cell death and include not only proteins but also DNA or lipids. Mitochondrial DAMPs induce inflammatory responses and are critically involved in the pathogenesis of various diseases.
  
  
  BACKGROUND
  Recent studies elucidate the molecular mechanisms by which mitochondrial DAMPs are released and initiate immune responses by use of genetically modulated cells or animals. Importantly, the levels of mitochondrial DAMPs in patients are often associated with severity and prognosis of human diseases, such as infection, asthma, ischemic heart disease, and cancer.
  
  
  RESULTS
  Although mitochondrial DAMPs can represent proinflammatory molecules in various experimental models, their roles in human diseases may be multifunctional and complex. It remains unclear where and how mitochondrial DAMPs are liberated into extracellular spaces and exert their biological functions particularly in vivo. In addition, while mitochondria can secrete several types of DAMPs during cell death, the interaction of each mitochondrial DAMP (e.g., synergistic effects) remains unclear.
  
  
  CONCLUSIONS
  Regulation of mitochondrial DAMP-mediated immune responses may be important to alter the progression of human diseases. In addition, measuring mitochondrial DAMPs in patients may be clinically useful as biomarkers to predict prognosis or response to therapies. Further studies of the mechanisms by which mitochondrial DAMPs impact the initiation and progression of diseases may lead to the development of therapeutics specifically targeting this pathway. Antioxid.
authors.affiliation: 1 Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital , New York, New York.|2 Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical College , New York, New York.
authors.forename: Kiichi
authors.initials: K
authors.lastname: Nakahira
authors.affiliation: 1 Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital , New York, New York.|2 Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical College , New York, New York.
authors.forename: Shu
authors.initials: S
authors.lastname: Hisata
authors.affiliation: 1 Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College and New York-Presbyterian Hospital , New York, New York.|2 Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical College , New York, New York.
authors.forename: Augustine M K
authors.initials: AM
authors.lastname: Choi
mesh_terms: D000818:Animals; D004272:DNA, Mitochondrial / Q000378:metabolism; D005110:Extracellular Space / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D008928:Mitochondria / Q000235:genetics* / Q000378:metabolism*; D024101:Mitochondrial Proteins / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D004272:DNA, Mitochondrial; D024101:Mitochondrial Proteins