Journal
REDOX BIOLOGY
Volume 2, Issue -, Pages 206-210Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.redox.2013.12.026
Keywords
Reserve capacity; Oxidative stress; Metabolic shift; Biomarker; Leukocytes; Platelets
Categories
Funding
- American Heart Association: NIH T32 [T32HL07918]
- NIDDK Diabetic Complications Consortium [DK076169]
- O'Brien Center [P30 DK079337]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007918] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK079337, U24DK076169] Funding Source: NIH RePORTER
Ask authors/readers for more resources
The assessment of metabolic function in cells isolated from human blood for treatment and diagnosis of disease is a new and important area of translational research. It is now becoming clear that a broad range of pathologies which present clinically with symptoms predominantly in one organ, such as the brain or kidney, also modulate mitochondrial energetics in platelets and leukocytes allowing these cells to serve as the canary in the coal mine for bioenergetic dysfunction. This opens up the possibility that circulating platelets and leukocytes can sense metabolic stress in patients and serve as biomarkers of mitochondrial dysfunction in human pathologies such as diabetes, neurodegeneration and cardiovascular disease. In this overview we will describe how the utilization of glycolysis and oxidative phosphorylation differs in platelets and leukocytes and discuss how they can be used in patient populations. Since it is clear that the metabolic programs between leukocytes and platelets are fundamentally distinct the measurement of mitochondrial function in distinct cell populations is necessary for translational research. (C) 2014 The Authors. Published by Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available