Mitochondrial signaling in the vascular endothelium: beyond reactive oxygen species. Basic Res Cardiol 2016 May;111(3):26
Date
03/20/2016Pubmed ID
26992928Pubmed Central ID
PMC6749826DOI
10.1007/s00395-016-0546-5Scopus ID
2-s2.0-84961777268 (requires institutional sign-in at Scopus site) 45 CitationsAbstract
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.
Author List
Kadlec AO, Beyer AM, Ait-Aissa K, Gutterman DDAuthors
Andreas M. Beyer PhD Professor in the Medicine department at Medical College of WisconsinDavid Gutterman MD Emeritus Professor in the Medicine department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsEndothelium, Vascular
Humans
Mitochondria
Reactive Oxygen Species
Signal Transduction
