Journal
BASIC RESEARCH IN CARDIOLOGY
Volume 111, Issue 3, Pages -Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00395-016-0546-5
Keywords
Mitochondria; Cardiovascular disease; Endothelium; Reactive oxygen species
Categories
Funding
- NHLBI NIH HHS [R01 HL113612] Funding Source: Medline
- NIGMS NIH HHS [T32 GM080202] Funding Source: Medline
- NIH HHS [R21 OD018306] Funding Source: Medline
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Traditionally, the mitochondria have been viewed as the cell's powerhouse, producing energy in the form of ATP. As a byproduct of ATP formation, the mitochondrial electron transport chain produces substantial amounts of reactive oxygen species (ROS). First thought to be toxic, recent literature indicates an important signaling function for mitochondria-derived ROS, especially in relation to cardiovascular disease pathogenesis. This has spawned an evolution to a more contemporary view of mitochondrial function as a dynamic organelle involved in key regulatory and cell survival processes. Beyond ROS, recent studies have identified a host of mitochondria-linked factors that influence the cellular and extracellular environments, including mitochondria-derived peptides, mitochondria-localized proteins, and the mitochondrial genome itself. Interestingly, many of these factors help orchestrate ROS homeostasis and ROS-related signaling. The paradigm defining the role of mitochondria in the vasculature needs to be updated yet again to include these key signaling factors, which serves as the focus of the current review. In describing these novel signaling factors, we pay specific attention to their influence on endothelial homeostasis. Therapies targeting these pathways are discussed, as are emerging research directions.
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