Cited by 42Mitochondrial Function and PathologyMetabolism and Genetic DisordersAutophagy in Disease and Therapy

Mitochondrial reactive oxygen species generation by the SDHC V69E mutation causes low birth weight and neonatal growth retardation

Ishii, Takamasa, Miyazawa, Masaki, Onodera, Akira, Yasuda, Kayo, Kawabe, Noboru, Kirinashizawa, Mika, Yoshimura, Shinichi, Maruyama, Naoki +2 more·2011·Mitochondrion

Abstract

We have previously demonstrated that excessive mitochondrial reactive oxygen species caused by mutations in the SDHC subunit of Complex II resulted in premature death in C. elegans and Drosophila, tumors in mouse cells and infertility in transgenic mice. We now report the generation and initial characterization of conditional transgenic mice (Tet-mev-1) using our uniquely developed Tet-On/Off system, which equilibrates transgene expression to endogenous levels. The mice experienced mitochondrial respiratory chain dysfunction that induced reactive oxygen species overproduction. The mitochondrial oxidative stress resulted in excessive apoptosis leading to low birth weight and growth retardation in the neonatal developmental phase in Tet-mev-1 mice.

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Crossref · 10.1016/j.mito.2010.09.006

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Authors
Ishii, T., Miyazawa, M., Onodera, A., Yasuda, K., Kawabe, N., Kirinashizawa, M., Yoshimura, S., Maruyama, N., Hartman, P. S., & Ishii, N.
Affiliations
  • Tokai University (JP)
  • Tokyo Metropolitan Institute of Gerontology (JP)
  • Texas Christian University (US)
Corresponding author
Ishii, Naoaki
Venue
Mitochondrion
Publisher
Elsevier BV
Published
2011-01
Volume
11
Issue
1
Pages
155-165
ISSN
1567-7249 (ISSN-L)
OpenAlex
W1989368620
Cited by
42
References
32
Citations by year
2026: 1 · 2025: 4 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 5 · 2015: 2 · 2014: 6 · 2013: 4 · 2012: 5
FWCI
1.56
Type
journal article
Language
en
Open access
closed
Locations
  • Mitochondrion (publishedVersion)
  • PubMed (publishedVersion)
Funders
Japan Society for the Promotion of Science (22510064)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
succinate dehydrogenase, reactive oxygen species, oxidative stress, mitochondrial respiratory chain dysfunction, apoptosis, low birth weight, mev-1, premature mortality
MeSH terms
Animals, Animals, Newborn, Disease Models, Animal, Gene Expression Regulation, Growth Disorders, Humans, Infant, Low Birth Weight, Infant, Newborn, Mice, Transgenic, Mitochondria, Mutation, Succinate Dehydrogenase, Tetracycline, Reactive Oxygen Species, Transgenes, Mitochondrial Diseases, NIH 3T3 Cells, Mice

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