Impaired endothelial function contributes to cardiac dysfunction: role of mitochondrial dynamics. Am J Physiol Heart Circ Physiol 2025 Jan 01;328(1):H29-H36
Date
11/19/2024Pubmed ID
39560973Pubmed Central ID
PMC12147231DOI
10.1152/ajpheart.00531.2024Scopus ID
2-s2.0-85212326562 (requires institutional sign-in at Scopus site) 1 CitationAbstract
The endothelial microvasculature is essential for the regulation of vasodilation and vasoconstriction, and improved functioning of the endothelium is linked to improved outcomes for individuals with coronary artery disease (CAD). People with endothelial dysfunction exhibit a loss of nitric oxide (NO)-mediated vasodilation, achieving vasodilation instead through mitochondria-derived H2O2. Mitochondrial dynamics is an important autoregulatory mechanism that contributes to mitochondrial and endothelial homeostasis and plays a role in the formation of reactive oxygen species (ROS), including H2O2. Dysregulation of mitochondrial dynamics leads to increased ROS production, decreased ATP production, impaired metabolism, activation of pathological signal transduction, impaired calcium sensing, and inflammation. We hypothesize that dysregulation of endothelial mitochondrial dynamics plays a crucial role in the endothelial microvascular dysfunction seen in individuals with CAD. Therefore, proper regulation of endothelial mitochondrial dynamics may be a suitable treatment for individuals with endothelial microvascular dysfunction, and we furthermore postulate that improving this microvascular dysfunction will directly improve outcomes for those with CAD.
Author List
Gutierrez-Huerta CA, Quiroz-Delfi G, Faleel FDM, Beyer AMAuthor
Andreas M. Beyer PhD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCoronary Artery Disease
Endothelial Cells
Endothelium, Vascular
Humans
Mitochondria
Mitochondria, Heart
Mitochondrial Dynamics
Nitric Oxide
Reactive Oxygen Species
Vasodilation
