ArticlePloS one2016
Cardiac Dysfunction in the BACHD Mouse Model of Huntington's Disease.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Systemic Symptoms in Huntington's Disease: A Comprehensive Review.Movement disorders clinical practice · 2024Pooled it
- Beyond the brain: Polyglutamine disease pathology outside the nervous system.Neurobiology of disease · 2026Review
- Sex-dependent mild cardiac dysfunction and neurometabolic abnormalities in a model of Huntington's disease.Disease models & mechanisms · 2026Article
- Fasciola hepatica-Derived Proteins Shield the Heart From Type 2 Myocardial Infarction in Rats by Modulating Oxidative Stress and Inflammatory Imbalance: Insights Relevant to the Hygiene Hypothesis.Oxidative medicine and cellular longevity · 2026Article
- Concomitant pathologies and their impact on Huntington's disease. A brief review of current evidence.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Atrial fibrillation risk model based on LASSO and SVM algorithms and immune infiltration of key mitochondrial energy metabolism genes.Scientific reports · 2025Article
- Brain-derived extracellular vesicles potentially mediate crosstalk with peripheral organs in neurodegenerative diseases.Frontiers in cell and developmental biology · 2025Review
- Differential response of neurons to autophagy modulation in Huntington's disease.Autophagy reports · 2025Article
- Review
- Scheduled feeding improves sleep in a mouse model of Huntington's disease.bioRxiv : the preprint server for biology · 2024Article
- Scheduled feeding improves sleep in a mouse model of Huntington's disease.Frontiers in neuroscience · 2024Article
- The lipolysis inhibitor acipimox reverses the cardiac phenotype induced by electronic cigarettes.Scientific reports · 2023Article
- Metabolism in Huntington's disease: a major contributor to pathology.Metabolic brain disease · 2022Review
- A New Perspective on Huntington's Disease: How a Neurological Disorder Influences the Peripheral Tissues.International journal of molecular sciences · 2022Review
- Huntington's disease phenotypes are improved via mTORC1 modulation by small molecule therapy.PloS one · 2022Article
- Systemic manifestation and contribution of peripheral tissues to Huntington's disease pathogenesis.Ageing research reviews · 2021Review
- Targeted Genetic Reduction of Mutant Huntingtin Lessens Cardiac Pathology in the BACHD Mouse Model of Huntington's Disease.Frontiers in cardiovascular medicine · 2021Article
- Progressive cardiac arrhythmias and ECG abnormalities in the Huntington's disease BACHD mouse model.Human molecular genetics · 2020Article
- Circadian dysfunction in the Q175 model of Huntington's disease: Network analysis.Journal of neuroscience research · 2019Article
- Chronic intermittent electronic cigarette exposure induces cardiac dysfunction and atherosclerosis in apolipoprotein-E knockout mice.American journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
While Huntington's disease (HD) is classified as a neurological disorder, HD patients exhibit a high incidence of cardiovascular events leading to heart failure and death. In this study, we sought to better understand the cardiovascular phenotype of HD using the BACHD mouse model. The age-related decline in cardiovascular function was assessed by echocardiograms, electrocardiograms, histological and microarray analysis. We found that structural and functional differences between WT and BACHD hearts start at 3 months of age and continue throughout life. The aged BACHD mice develop cardiac fibrosis and ultimately apoptosis. The BACHD mice exhibited adaptive physiological changes to chronic isoproterenol treatment; however, the medication exacerbated fibrotic lesions in the heart. Gene expression analysis indicated a strong tilt toward apoptosis in the young mutant heart as well as changes in genes involved in cellular metabolism and proliferation. With age, the number of genes with altered expression increased with the large changes occurring in the cardiovascular disease, cellular metabolism, and cellular transport clusters. The BACHD model of HD exhibits a number of changes in cardiovascular function that start early in the disease progress and may provide an explanation for the higher cardiovascular risk in HD.
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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.