Mitochondrial fission mediates high glucose-induced cell death through elevated production of reactive oxygen species
Open accessAbstract
AIMS: One of the main causes of cardiovascular complications in diabetes is the hyperglycaemia-induced cell injury, and mitochondrial fission has been implicated in the apoptotic process. We investigated the role of mitochondrial fission in high glucose-induced cardiovascular cell injury. METHODS AND RESULTS: We used several types of cultured mouse, rat, and bovine cells from the cardiovascular system, and evaluated mitochondrial morphology, reactive oxygen species (ROS) levels, and apoptotic parameters in sustained high glucose incubation. Adenoviral infection was used for the inhibition of the fission protein DLP1. We found that mitochondria were short and fragmented in cells incubated in sustained high glucose conditions. Under the same conditions, cellular ROS levels were high and cell death was increased. We demonstrated that the increased level of ROS causes mitochondrial permeability transition (MPT), phosphatidylserine exposure, cytochrome c release, and caspase activation in prolonged high glucose conditions. Importantly, maintaining tubular mitochondria by inhibiting mitochondrial fission in sustained high glucose conditions normalized cellular ROS levels and prevented the MPT and subsequent cell death. These results demonstrate that mitochondrial fragmentation is an upstream factor for ROS overproduction and cell death in prolonged high glucose conditions. CONCLUSION: These findings indicate that the fission-mediated fragmentation of mitochondrial tubules is causally associated with enhanced production of mitochondrial ROS and cardiovascular cell injury in hyperglycaemic conditions.
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Several types of cultured cells from the cardiovascular system exhibited mitochondrial fission under hyperglycemic conditions.
“Several types of cultured cells from the cardiovascular system exhibited mitochondrial fission under hyperglycemic conditions (48).”
From Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2012) · cites this paper as [48]
Many studies demonstrated effect of hyperglycemia on increased generation of ROS and mitochondrial fission in a variety of cell types.
“Although many studies demonstrated the effect of hyperglycemia on increased generation of ROS and mitochondrial fission in a variety of cell types (26, 48), elevated circulating lipid and inflammatory cytokines usually occur prior to the development of hyperinsulinemia and hyperglycemia during the progression of type 2 diabetes (27, 38).”
From Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2012) · cites this paper as [48]
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“mitochondrial morphology affecting mitochondrial function (Chen et al., 2005;Jahani-Asl et al., 2007;Yu et al., 2008;Ong et al., 2010;Gomes et al., 2011) and vice versa (Benard et al.”
BackgroundMitochondrial dynamics in skeletal muscle insulin resistance and type 2 diabetes
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- Authors
- Yu, T., Sheu, S.-S., Robotham, J. L., & Yoon, Y.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- Yoon, Yisang
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-04-25
- Volume
- 79
- Issue
- 2
- Pages
- 341-351
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC2646899
- OpenAlex
- W2131666074
- Cited by
- 462
- References
- 52
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 31 · 2023: 25 · 2022: 25 · 2021: 31 · 2020: 31 · 2019: 23 · 2018: 37 · 2017: 33 · 2016: 36 · 2015: 26 · 2014: 25 · 2013: 22 · 2012: 34
- FWCI
- 8.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Medical Center, University of Rochester
- National Heart, Lung, and Blood Institute (HL033333, R01HL033333)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK078618, R21DK073858, DK 078618, DK073858)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial fission, high glucose, reactive oxygen species, mitochondrial permeability transition, apoptosis, mitochondrial fragmentation, diabetes mellitus, caspase activation, cytochrome c release, phosphatidylserine exposure, hyperglycemia
- MeSH terms
- Animals, Aorta, Cattle, Cells, Cultured, Disease Models, Animal, Dose-Response Relationship, Drug, Endothelium, Vascular, Glucose, Hyperglycemia, Mitochondria, Heart, Apoptosis, Reactive Oxygen Species, Myocytes, Cardiac, Dynamin I, Mice, Rats
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