ArticleThe Biochemical journal2013
Mitochondrial genetic background modulates bioenergetics and susceptibility to acute cardiac volume overload.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 94 citations in OpenAlex.
- Mitochondrial Genetic Background Shapes Baseline Retinal Function, Age-Related Bioenergetic Remodeling, and Microglial STING Phenotypes.Aging cell · 2026Article
- Mitochondrial tRNA-Derived Fragments as Candidate Metastasis-Modifying RNA.Cancer research communications · 2026Article
- Mitochondria and the epigenome: maternal co-inheritance and crosstalk from oocyte to embryo.Cell communication and signaling : CCS · 2026Review
- Mitochondrial haplotype and sex modulate responses to endurance exercise training.The Journal of physiology · 2025Article
- Multi-tissue metabolomics reveal mtDNA- and diet-specific metabolite profiles in a mouse model of cardiometabolic disease.Redox biology · 2025Article
- Mitochondrial DNA alterations in precision oncology: Emerging roles in diagnostics and therapeutics.Clinics (Sao Paulo, Brazil) · 2025Review
- Preclinical models of mitochondrial dysfunction: mtDNA and nuclear-encoded regulators in diverse pathologies.Frontiers in aging · 2025Review
- Increased Diabetes Complications in a Mouse Model of Oxidative Stress Due to 'Mismatched' Mitochondrial DNA.Antioxidants (Basel, Switzerland) · 2024Article
- Mitochondrial Genetics and Function as Determinants of Bone Phenotype and Aging.Current osteoporosis reports · 2023Review
- Mitochondrial Transfer to Host Cells from Ex Vivo Expanded Donor Hematopoietic Stem Cells.Cells · 2023Article
- A Genetically Heterogeneous Rat Model with Divergent Mitochondrial Genomes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- Thyroid hormone modulates hyperoxic neonatal lung injury and mitochondrial function.JCI insight · 2023Article
- Mitochondrial haplotype modulates genome expression and mitochondrial structure/function in cardiomyocytes following volume overload.American journal of physiology. Heart and circulatory physiology · 2023Article
- Generating Mitochondrial-Nuclear Exchange (MNX) Mice to Identify Mitochondrial Determinants of Cancer Metastasis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Roles of mitochondrial genetics in cancer metastasis.Trends in cancer · 2022Review
- Inefficient Batteries in Heart Failure: Metabolic Bottlenecks Disrupting the Mitochondrial Ecosystem.JACC. Basic to translational science · 2022Review
- Increased mtDNA mutation frequency in oocytes causes epigenetic alterations and embryonic defects.National science review · 2022Article
- Mitochondrial TrxR2 regulates metabolism and protects from metabolic disease through enhanced TCA and ETC function.Communications biology · 2022Article
- Mechanisms of breast cancer metastasis.Clinical & experimental metastasis · 2022Review
- Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
20 authors at 3 institutions in 1 country.
Funding
Abstract
Dysfunctional bioenergetics has emerged as a key feature in many chronic pathologies such as diabetes and cardiovascular disease. This has led to the mitochondrial paradigm in which it has been proposed that mtDNA sequence variation contributes to disease susceptibility. In the present study we show a novel animal model of mtDNA polymorphisms, the MNX (mitochondrial-nuclear exchange) mouse, in which the mtDNA from the C3H/HeN mouse has been inserted on to the C57/BL6 nuclear background and vice versa to test this concept. Our data show a major contribution of the C57/BL6 mtDNA to the susceptibility to the pathological stress of cardiac volume overload which is independent of the nuclear background. Mitochondria harbouring the C57/BL6J mtDNA generate more ROS (reactive oxygen species) and have a higher mitochondrial membrane potential relative to those with C3H/HeN mtDNA, independent of nuclear background. We propose this is the primary mechanism associated with increased bioenergetic dysfunction in response to volume overload. In summary, these studies support the 'mitochondrial paradigm' for the development of disease susceptibility, and show that the mtDNA modulates cellular bioenergetics, mitochondrial ROS generation and susceptibility to cardiac stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.