Mitochondrial Ca2+ transport in the endothelium: regulation by ions, redox signalling and mechanical forces

Calcium (Ca2+) transport by mitochondria is an important component of the cell Ca2+ homeostasis machinery in metazoans. Ca2+ uptake by mitochondria is a major determinant of bioenergetics and cell fate. Mitochondrial Ca2+ uptake occurs via the mitochondrial Ca2+ uniporter (MCU) complex, an inner mit...

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Bibliographic Details
Published in:Journal of the Royal Society interface 2017-12, Vol.14 (137), p.20170672-20170672
Main Authors: Alevriadou, B. Rita, Shanmughapriya, Santhanam, Patel, Akshar, Stathopulos, Peter B., Madesh, Muniswamy
Format: Article
Language:English
Subjects:
Arteries
Arteriosclerosis
Atherosclerosis
Bioenergetics
Calcium
Calcium (intracellular)
Calcium (mitochondrial)
Calcium homeostasis
Calcium influx
Calcium transport
Cell fate
Endothelial cells
Endothelium
Headline Review
Homeostasis
Machinery and equipment
Mechanotransduction
Membrane proteins
Mitochondria
Mitochondrial Ca
Proteins
Reactive Oxygen Species
Review
Review Articles
Shear Stress
Signaling
Transport
Uniporter
Vascular diseases
Vascular Endothelial Cell
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Summary:Calcium (Ca2+) transport by mitochondria is an important component of the cell Ca2+ homeostasis machinery in metazoans. Ca2+ uptake by mitochondria is a major determinant of bioenergetics and cell fate. Mitochondrial Ca2+ uptake occurs via the mitochondrial Ca2+ uniporter (MCU) complex, an inner mitochondrial membrane protein assembly consisting of the MCU Ca2+ channel, as its core component, and the MCU complex regulatory/auxiliary proteins. In this review, we summarize the current knowledge on the molecular nature of the MCU complex and its regulation by intra- and extramitochondrial levels of divalent ions and reactive oxygen species (ROS). Intracellular Ca2+ concentration ([Ca2+]i), mitochondrial Ca2+ concentration ([Ca2+]m) and mitochondrial ROS (mROS) are intricately coupled in regulating MCU activity. Here, we highlight the contribution of MCU activity to vascular endothelial cell (EC) function. Besides the ionic and oxidant regulation, ECs are continuously exposed to haemodynamic forces (either pulsatile or oscillatory fluid mechanical shear stresses, depending on the precise EC location within the arteries). Thus, we also propose an EC mechanotransduction-mediated regulation of MCU activity in the context of vascular physiology and atherosclerotic vascular disease.
ISSN:1742-5689
1742-5662
DOI:10.1098/rsif.2017.0672