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: Hiroyuki Nakayama, Kinya Otsu
• Journal: Trends in endocrinology and metabolism: TEM (Trends Endocrinol Metab) Vol. 24 Issue 11 Pg. 546-53 (Nov 2013) ISSN: 1879-3061 [Electronic] United States
• PMID: 23850260 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2013 Elsevier Ltd. All rights reserved.

Chemical References

• DNA, Mitochondrial
• Inflammasomes

Topics

• DNA, Mitochondrial (metabolism)
• Heart
• Heart Failure (metabolism)
• Hemodynamics
• Humans
• Inflammasomes (metabolism)
• Inflammation (metabolism)