ArticleReactive oxygen species (Apex, N.C.)2016
Huntington's Disease-Induced Cardiac Disorders Affect Multiple Cellular Pathways.
Article in Reactive oxygen species (Apex, N.C.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Systemic Symptoms in Huntington's Disease: A Comprehensive Review.Movement disorders clinical practice · 2024Pooled it
- An orally available, brain penetrant, small molecule lowers huntingtin levels by enhancing pseudoexon inclusion.Nature communications · 2022Trial
- Targeting the cGAS-STING pathway mitigates Huntington disease pathogenesis in a knock-in mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- An integrative neuropharmacological review of Huntington's disease challenges and the role of novel formulations in addressing pharmacological‒pharmaceutical limitations.Frontiers in pharmacology · 2026Review
- Heart-brain axis, gliotransmitters and peripheral neurogenesis: Emerging regenerative roles of cardiac nexus glia in health and disease.World journal of cardiology · 2025Review
- Concomitant pathologies and their impact on Huntington's disease. A brief review of current evidence.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Review
- Neurodegenerative disorders, metabolic icebergs, and mitohormesis.Translational neurodegeneration · 2024Review
- Circadian Interventions in Preclinical Models of Huntington's Disease: A Narrative Review.Biomedicines · 2024Review
- Modifiable factors associated with Huntington's disease progression in presymptomatic participants.Annals of clinical and translational neurology · 2024Observational
- Small Molecule Pytren-4QMn Metal Complex Slows down Huntington's Disease Progression in Male zQ175 Transgenic Mice.International journal of molecular sciences · 2023Article
- Normal range CAG repeat size variations in the HTT gene are associated with an adverse lipoprotein profile partially mediated by body mass index.Human molecular genetics · 2023Article
- 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
- Hypertension, Antihypertensive Use and the Delayed-Onset of Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2020Observational
- Progressive cardiac arrhythmias and ECG abnormalities in the Huntington's disease BACHD mouse model.Human molecular genetics · 2020Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) is a rare, inherited, progressive, and fatal neurological disorder resulting from expanded polyglutamine repeats in the huntingtin protein. While HD is predominately characterized as a disease of the central nervous system, mortality surveys and epidemiological studies reveal heart disease as one of the leading causes of death in HD patients. Emerging evidence supports a link between HD and cardiovascular disease, such as cardiac amyloidosis (accumulation of aggregates in the heart). Experimental animal and clinical studies have attempted to explain the mechanisms of HD-induced cardiac pathology in the association of protein misfolding, autophagic defects, oxidative stress, mitochondrial dysfunction, and cell death. HD is increasingly understood as a complex disease with peripheral components of cardiac and skeletal muscle pathophysiology. While the discovery of these linkages and apparent pathological markers is promising, the mechanism of HD-induced cardiac pathology and the nature of its cell autonomy remain elusive. Further study of the wide-ranging cardiac function in HD patients is needed. This review highlights published literature on the pathological factors associated with HD-induced cardiac amyloidosis and other cardiovascular diseases, and addresses gaps in this expanding area of study. Through comprehensive experimental and clinical studies, potential drugs can be tested to attenuate and/or ameliorate HD-induced cardiac pathology and mortality.
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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.