Journal article
Mitochondrial signaling in the vascular endothelium: beyond reactive oxygen species
Basic research in cardiology, Vol.111(3), pp.26-26
03/01/2016
DOI: 10.1007/s00395-016-0546-5
PMCID: PMC6749826
PMID: 26992928
Abstract
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.
Details
- Title: Subtitle
- Mitochondrial signaling in the vascular endothelium: beyond reactive oxygen species
- Creators
- Andrew O. Kadlec - Medical College of WisconsinAndreas M. Beyer - Medical College of WisconsinKarima Ait-Aissa - Medical College of WisconsinDavid D. Gutterman - Medical College of Wisconsin
- Resource Type
- Journal article
- Publication Details
- Basic research in cardiology, Vol.111(3), pp.26-26
- DOI
- 10.1007/s00395-016-0546-5
- PMID
- 26992928
- PMCID
- PMC6749826
- NLM abbreviation
- Basic Res Cardiol
- ISSN
- 0300-8428
- eISSN
- 1435-1803
- Publisher
- Springer Nature
- Number of pages
- 12
- Grant note
- R01 HL113612 / NHLBI NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) T32 GM080202 / NIGMS NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of General Medical Sciences (NIGMS) R21 OD018306 / NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA
- Language
- English
- Date published
- 03/01/2016
- Academic Unit
- Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984359819302771
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