ReviewLaboratory investigation; a journal of technical methods and pathology2011
The mitochondrial paradigm for cardiovascular disease susceptibility and cellular function: a complementary concept to Mendelian genetics.
Review in Laboratory investigation; a journal of technical methods and pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Multi-tissue metabolomics reveal mtDNA- and diet-specific metabolite profiles in a mouse model of cardiometabolic disease.Redox biology · 2025Article
- The landscape of rare mitochondrial DNA variants in sudden cardiac death: A potential role for ATP synthase.Heliyon · 2025Article
- Emerging roles of mitochondrial functions and epigenetic changes in the modulation of stem cell fate.Cellular and molecular life sciences : CMLS · 2024Review
- The Determination of Mitochondrial Mass Is a Prerequisite for Accurate Assessment of Peripheral Blood Mononuclear Cells' Oxidative Metabolism.International journal of molecular sciences · 2023Article
- Examining the Association between Mitochondrial Genome Variation and Coronary Artery Disease.Genes · 2022Article
- The role of mitochondria in the pathogenesis of Kawasaki disease.Frontiers in immunology · 2022Article
- Mito-Mendelian interactions alter in vivo glucose metabolism and insulin sensitivity in healthy mice.American journal of physiology. Endocrinology and metabolism · 2021Article
- Cardiac complications in inherited mitochondrial diseases.Heart failure reviews · 2021Review
- Mitochondrial DNA Depletion Syndrome and Its Associated Cardiac Disease.Frontiers in cardiovascular medicine · 2021Review
- An evolutionary, or "Mitocentric" perspective on cellular function and disease.Redox biology · 2020Review
- Blood-based bioenergetics: An emerging translational and clinical tool.Molecular aspects of medicine · 2020Review
- Sex Hormone Regulation of Proteins Modulating Mitochondrial Metabolism, Dynamics and Inter-Organellar Cross Talk in Cardiovascular Disease.Frontiers in cell and developmental biology · 2020Review
- Bioenergetics and translational metabolism: implications for genetics, physiology and precision medicine.Biological chemistry · 2019Review
- Review
- Mitochondrial genetic haplogroups and cardiovascular diseases: Data from the Osteoarthritis Initiative.PloS one · 2019Article
- UPRCell research · 2018Review
- Quercetin Prevents Diastolic Dysfunction Induced by a High-Cholesterol Diet: Role of Oxidative Stress and Bioenergetics in Hyperglycemic Rats.Oxidative medicine and cellular longevity · 2018Article
- Mitochondrial DNA mutations and cardiovascular disease.Current opinion in cardiology · 2017Article
- Mitochondrial Nucleoid: Shield and Switch of the Mitochondrial Genome.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
While there is general agreement that cardiovascular disease (CVD) development is influenced by a combination of genetic, environmental, and behavioral contributors, the actual mechanistic basis of how these factors initiate or promote CVD development in some individuals while others with identical risk profiles do not, is not clearly understood. This review considers the potential role for mitochondrial genetics and function in determining CVD susceptibility from the standpoint that the original features that molded cellular function were based upon mitochondrial-nuclear relationships established millions of years ago and were likely refined during prehistoric environmental selection events that today, are largely absent. Consequently, contemporary risk factors that influence our susceptibility to a variety of age-related diseases, including CVD were probably not part of the dynamics that defined the processes of mitochondrial-nuclear interaction, and thus, cell function. In this regard, the selective conditions that contributed to cellular functionality and evolution should be given more consideration when interpreting and designing experimental data and strategies. Finally, future studies that probe beyond epidemiologic associations are required. These studies will serve as the initial steps for addressing the provocative concept that contemporary human disease susceptibility is the result of selection events for mitochondrial function that increased chances for prehistoric human survival and reproductive success.
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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.