Hypoxemia Is Associated With Mitochondrial DNA Damage and Gene Induction: Implications for Cardiac Disease
Abstract
Objective --Oxidative phosphorylation (OXPHOS) deficiency due to hypoxemia or other causes was hypothesized to increase oxygen radical generation, damage mitochondrial DNA (mtDNA), and reduce adenosine triphosphate synthesis, resulting in compensatory OXPHOS gene induction. Therefore, we investigated the levels of mtDNA damage and OXPHOS transcripts in normal and ischemic hearts, and then in other forms of heart disease.Design --DNA was extracted from the heart and the levels of the common 4977 base pair mtDNA deletion were quantitated as an index for mtDNA damage. Total RNA was extracted from hearts and analyzed for OXPHOS transcript levels.Results --In control hearts, the 4977 base pair mtDNA deletion appeared at age 40 years and reached a maximum deletion of 0.0035%. Much higher levels were found in ischemic hearts (0.02% to 0.85%), as well as in three of 10 cases with other types of heart disease (0.017% to 0.16%). The OXPHOS transcripts were increased in all diseased hearts.Conclusion --Ischemic hearts have increased mtDNA damage and OXPHOS gene expression, suggesting that mtDNA damage is associated with OXPHOS deficiency. Oxidative phosphorylation defects may also play a role in some other forms of cardiac disease.
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mtDNA mutations are associated with atherosclerosis, hypertension, type 2 diabetes, cardiovascular disease, and obesity.
“Moreover, mtDNA mutations have been associated with the development of chronic human diseases, such as atherosclerosis, hypertension, T2DM, cardiovascular disease and obesity175–178.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [177]
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Decreased NADH dehydrogenase and ubiquinol-cytochromecoxidoreductase in peripheral arterial disease
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Identification of cystic fibrosis mutations in the United Arab Emirates
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Specific mitochondrial DNA deletions in idiopathic dilated cardiomyopathy.
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“For example, the deletion estimate of one group [ 8 ] is 2-3 orders of magnitude lower than that observed by others [5,10].”
BackgroundMethodNuclear respiratory factors and the pathways of nuclear-mitochondrial interaction.
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“Finally, ischemic hearts have been found to accumulate mtDNA deletions at a higher frequency than normal and also to have elevated expression of certain nuclear genes involved in oxidative phosphorylation (Corral-Debrinski et al. 1991).”
BackgroundMolecular and biochemical changes of the cardiovascular system due to smoking exposure
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- Authors
- Corral-Debrinski, M.
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 1991-10-02
- Volume
- 266
- Issue
- 13
- Pages
- 1812
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- OpenAlex
- W7214182327
- Cited by
- 1
- References
- 0
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- JAMA (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › High Altitude and Hypoxia
- Keywords
- hypoxemia, mitochondrial DNA damage, gene induction, oxidative stress
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