The on-off switches of the mitochondrial uncoupling proteins
Open accessAbstract
Mitochondrial uncoupling proteins disengage substrate oxidation from ADP phosphorylation by dissipating the proton electrochemical gradient that is required for ATP synthesis. In doing this, the archetypal uncoupling protein, UCP1, mediates adaptive thermogenesis. By contrast, its paralogues UCP2 and UCP3 are not thought to mediate whole body thermogenesis in mammals. Instead, they have been implicated in a variety of physiological and pathological processes, including protection from oxidative stress, negative regulation of glucose sensing systems and the adaptation of fatty acid oxidation capacity to starving. Although much work has been devoted to how these proteins are activated, little is known of the mechanisms that reverse this activation.
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UCPs lessen mitochondrial ROS formation by lowering mitochondrial membrane potential by increasing proton leak from the intermembrane space back into the matrix.
“These anion carriers lessen mitochondrial ROS formation by lowering the mitochondrial membrane potential by increasing the leak of protons from the intermembrane space back into the matrix, a process that also occurs to some extent through the ANT (22).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [22]
Upregulation of UCP expression or activation lessens mitochondrial oxidant production.
“Upregulation of UCP expression or activation can also lessen mitochondrial oxidant production (22).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [22]
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References 74 · Cited by 239
- Authors
- Azzu, V., & Brand, M. D.
- Affiliations
- MRC Mitochondrial Biology Unit (GB)
- Buck Institute for Research on Aging (US)
- Corresponding author
- Azzu, Vian
- Venue
- Trends in Biochemical Sciences
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 35
- Issue
- 5
- Pages
- 298-307
- ISSN
- 0968-0004 (ISSN-L)
- PMC
- PMC3640847
- OpenAlex
- W2112947221
- Cited by
- 239
- References
- 74
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 9 · 2023: 9 · 2022: 13 · 2021: 13 · 2020: 14 · 2019: 13 · 2018: 18 · 2017: 15 · 2016: 19 · 2015: 13 · 2014: 21 · 2013: 23 · 2012: 20
- FWCI
- 1.22
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Trends in Biochemical Sciences (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Medical Research Council
- National Institute on Aging (PL1AG032118, P01AG025901, P30AG025708)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
- Keywords
- mitochondrial uncoupling proteins, UCP1, UCP2, UCP3, proton gradient, thermogenesis, oxidative stress, glucose detection, fatty acid oxidation, ATP production
- MeSH terms
- Acclimatization, Animals, Humans, Mitochondria, Proteins, Thermogenesis, Lipid Metabolism
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