title: Translation of hemodynamic stress to sterile inflammation in the heart.
abstract: Recently, growing evidence suggests that cardiac inflammation contributes to progression of heart failure (HF). However, the precise mechanism has been elusive. Autophagy is well-known phenomenon which plays essential roles in the maintenance of cardiomyocyte homeostasis by clearing damaged proteins and organelles, and dysfunction of this system evokes HF. Although emerging roles of mitochondria in inflammasome development are highlighted in immune cells, an involvement in the heart has not been defined until recently. This review discusses recent advances in understanding the complex mechanisms underlying cardiac inflammation: these studies have revealed that a combination of mitochondrial autophagy and innate immune responses to mitochondrial DNA during increased hemodynamic stress contribute to cardiac inflammation.
authors.affiliation: Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka 565-0871, Japan.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nakayama
authors.forename: Kinya
authors.initials: K
authors.lastname: Otsu
mesh_terms: D004272:DNA, Mitochondrial / Q000378:metabolism; D006321:Heart; D006333:Heart Failure / Q000378:metabolism; D006439:Hemodynamics; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*
chemical_list: D004272:DNA, Mitochondrial; D058847:Inflammasomes
keywords: DNase II; TLR9; autophagy; heart failure; inflammation; mitochondrion