ArticleJournal of biomechanics2015
Mitochondria DNA mutations cause sex-dependent development of hypertension and alterations in cardiovascular function.
Article in Journal of biomechanics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- The longevity effects of reduced IGF-1 signaling depend on the stability of the mitochondrial genome.Science advances · 2026Article
- Mitochondria, Sex, and Cardiovascular Disease: A Complex Interplay.International journal of molecular sciences · 2025Review
- Review
- Vitamin B12 status and folic acid supplementation influence mitochondrial heteroplasmy levels in mice.PNAS nexus · 2024Article
- Loss-of-function mitochondrial DNA polymerase gamma variants cause vascular smooth muscle cells to secrete a diffusible mitogenic factor.Frontiers in physiology · 2024Article
- mt-tRNAs in the polymerase gamma mutant heart.The journal of cardiovascular aging · 2023Article
- Cardiovascular aging: from cellular and molecular changes to therapeutic interventions.The journal of cardiovascular aging · 2023Article
- Mito-SiPE is a sequence-independent and PCR-free mtDNA enrichment method for accurate ultra-deep mitochondrial sequencing.Communications biology · 2022Article
- Molecular signature of cardiac remodeling associated with Polymerase Gamma mutation.Life sciences · 2022Article
- Flow-induced endothelial mitochondrial remodeling mitigates mitochondrial reactive oxygen species production and promotes mitochondrial DNA integrity in a p53-dependent manner.Redox biology · 2022Article
- Mitochondrial contributions to vascular endothelial dysfunction, arterial stiffness, and cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2021Review
- The Role of Mitochondria in Vascular Calcification.Journal of translational internal medicine · 2020Review
- Pulmonary vascular mechanical consequences of ischemic heart failure and implications for right ventricular function.American journal of physiology. Heart and circulatory physiology · 2019Article
- Beneficial effects of mesenchymal stem cell delivery via a novel cardiac bioscaffold on right ventricles of pulmonary arterial hypertensive rats.American journal of physiology. Heart and circulatory physiology · 2019Article
- Cardiovascular function and structure are preserved despite induced ablation of BMP1-related proteinases.Cellular and molecular bioengineering · 2018Article
- Inherited mitochondrial genomic instability and chemical exposures.Toxicology · 2017Review
- Right Ventricular-Pulmonary Vascular Interactions.Physiology (Bethesda, Md.) · 2017Review
- Mitochondrial DNA 3243A>G heteroplasmy is associated with changes in cytoskeletal protein expression and cell mechanics.Journal of the Royal Society, Interface · 2017Article
- Pulmonary arterial strain- and remodeling-induced stiffening are differentiated in a chronic model of pulmonary hypertension.Journal of biomechanics · 2017Article
- Limiting collagen turnover via collagenase-resistance attenuates right ventricular dysfunction and fibrosis in pulmonary arterial hypertension.Physiological reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Aging is associated with conduit artery stiffening that is a risk factor for and can precede hypertension and ventricular dysfunction. Increases in mitochondria DNA (mtDNA) frequency have been correlated with aging. Mice with a mutation in the encoding domain (D257A) of a proof-reading deficient version of mtDNA polymerase-γ (POLG) have musculoskeletal features of premature aging and a shortened lifespan. However, few studies using these mice have investigated the effects of mtDNA mutations on cardiovascular function. We hypothesized that the proof-reading deficient mtDNA POLG leads to arterial stiffening, hypertension, and ventricular hypertrophy. Ten to twelve month-old D257A mice (n=13) and age- and sex-matched wild-type controls (n=13) were catheterized for hemodynamic and ventricular function measurements. Left common carotid arteries (LCCA) were harvested for mechanical tests followed by histology. Male D257A mice had pulmonary and systemic hypertension, arterial stiffening, larger LCCA diameter (701±45 vs. 597±60μm), shorter LCCA axial length (8.96±0.56 vs. 10.10±0.80mm), and reduced hematocrit (29.1±6.1 vs. 41.3±8.1; all p<0.05). Male and female D257A mice had biventricular hypertrophy (p<0.05). Female D257A mice did not have significant increases in pressure or arterial stiffening, suggesting that the mechanisms of hypertension or arterial stiffening from mtDNA mutations differ based on sex. Our results lend insight into the mechanisms of age-related cardiovascular disease and may point to novel treatment strategies to address cardiovascular mortality in the elderly.
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Registered trials
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