The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Suppressors of Superoxide-H 2 O 2 Production at Site I Q of Mitochondrial Complex I Protect against Stem Cell Hyperplasia and Ischemia-Reperfusion Injury
Open accessAbstract
Using high-throughput screening we identified small molecules that suppress superoxide and/or H 2 O 2 production during reverse electron transport through mitochondrial respiratory complex I (site I Q) without affecting oxidative phosphorylation (suppressors of site I Q electron leak, "S1QELs"). S1QELs diminished endogenous oxidative damage in primary astrocytes cultured at ambient or low oxygen tension, showing that site I Q is a normal contributor to mitochondrial superoxide-H 2 O 2 production in cells. They diminished stem cell hyperplasia in Drosophila intestine in vivo and caspase activation in a cardiomyocyte cell model driven by endoplasmic reticulum stress, showing that superoxide-H 2 O 2 production by site I Q is involved in cellular stress signaling. They protected against ischemia-reperfusion injury in perfused mouse heart, showing directly that superoxide-H 2 O 2 production by site I Q is a major contributor to this pathology. S1QELs are tools for assessing the contribution of site I Q to cell physiology and pathology and have great potential as therapeutic leads.
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“Complex II is also capable of matrix mtROS production [100,101,102,103,104] and two different modes of production were described:”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [102]
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Chouchani, E. T., Pell, V. R., Gaude, E., Aksentijević, D., Sundier, S. Y., Robb, E. L., Logan, A., Nadtochiy, S. M., Ord, E. N. J., Smith, A. C., et al. (2014) · Nature · doi:10.1038/nature13909 · Cited by 2,907
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Chouchani, E. T., Pell, V. R., James, A. M., Work, L. M., Saeb-Parsy, K., Frezza, C., Krieg, T., & Murphy, M. P. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.12.009 · Cited by 752
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Metadata
- Authors
- Brand, M. D., Goncalves, R. L. S., Orr, A. L., Vargas, L., Gerencser, A. A., Borch Jensen, M., Wang, Y. T., Melov, S., Turk, C. N., Matzen, J. T., Dardov, V. J., Petrassi, H. M., Meeusen, S. L., Perevoshchikova, I. V., Jasper, H., Brookes, P. S., & Ainscow, E. K.
- Affiliations
- Buck Institute for Research on Aging (US)
- Genomics Institute of the Novartis Research Foundation (US)
- University of Rochester Medicine (US)
- Corresponding author
- Brand, Martin D.
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2016-10
- Volume
- 24
- Issue
- 4
- Pages
- 582-592
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC5061631
- OpenAlex
- W2522162634
- Cited by
- 228
- References
- 35
- Citations by year
- 2026: 22 · 2025: 25 · 2024: 26 · 2023: 23 · 2022: 23 · 2021: 31 · 2020: 29 · 2019: 20 · 2018: 15 · 2017: 14
- FWCI
- 8.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG033542, TL1AG032116)
- National Heart, Lung, and Blood Institute (R01HL127891)
- National Institute of General Medical Sciences (R01GM100196)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial complex I, reverse electron transfer, superoxide production, hydrogen peroxide production, electron leak, small molecule screening, intestinal stem cells, Drosophila intestine, endoplasmic reticulum stress, caspase activation, cardiomyocytes, ischemia-reperfusion injury, heart, astrocytes, oxidative stress
- MeSH terms
- Animals, Astrocytes, Cells, Cultured, Drosophila, Heart, Hydrogen Peroxide, Hyperplasia, Intestines, Mitochondria, Muscle, Oxidative Phosphorylation, Perfusion, Stem Cells, Superoxides, Tunicamycin, Reperfusion Injury, Oxidative Stress, Cytoprotection, Electron Transport Complex I, Cell Proliferation, Mice, Rats, Caspase 3, Caspase 7
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