ArticlePLoS genetics2017
Age-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Dual color optogenetic tool enables heart arrest, bradycardic, and tachycardic pacing in Drosophila melanogaster.Communications biology · 2024Article
- The nutrient sensor CRTC and Sarcalumenin/thinman represent an alternate pathway in cardiac hypertrophy.Cell reports · 2024Article
- Multiplatform modeling of atrial fibrillation identifies phospholamban as a central regulator of cardiac rhythm.Disease models & mechanisms · 2023Article
- Early Divergence of the C-Terminal Variable Region of Troponin T Via a Pair of Mutually Exclusive Alternatively Spliced Exons Followed by a Selective Fixation in Vertebrate Heart.Journal of molecular evolution · 2022Article
- Atrial Fibrillation Genomics: Discovery and Translation.Current cardiology reports · 2021Review
- Conserved Role of the Large Conductance Calcium-Activated Potassium Channel, KCirculation. Genomic and precision medicine · 2021Article
- Prolonged Exposure to Microgravity Reduces Cardiac Contractility and Initiates Remodeling in Drosophila.Cell reports · 2020Article
- The environmental toxicant ziram enhances neurotransmitter release and increases neuronal excitability via the EAG family of potassium channels.Neurobiology of disease · 2020Article
- Silencing of CCR4-NOT complex subunits affects heart structure and function.Disease models & mechanisms · 2020Article
- The Drosophila ERG channel seizure plays a role in the neuronal homeostatic stress response.PLoS genetics · 2019Article
- Conservation of cardiac L-type CaJournal of molecular and cellular cardiology · 2018Article
- The Light and Shadow of Senescence and Inflammation in Cardiovascular Pathology and Regenerative Medicine.Mediators of inflammation · 2017Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Understanding the cellular-molecular substrates of heart disease is key to the development of cardiac specific therapies and to the prevention of off-target effects by non-cardiac targeted drugs. One of the primary targets for therapeutic intervention has been the human ether a go-go (hERG) K+ channel that, together with the KCNQ channel, controls the rate and efficiency of repolarization in human myocardial cells. Neither of these channels plays a major role in adult mouse heart function; however, we show here that the hERG homolog seizure (sei), along with KCNQ, both contribute significantly to adult heart function as they do in humans. In Drosophila, mutations in or cardiac knockdown of sei channels cause arrhythmias that become progressively more severe with age. Intracellular recordings of semi-intact heart preparations revealed that these perturbations also cause electrical remodeling that is reminiscent of the early afterdepolarizations seen in human myocardial cells defective in these channels. In contrast to KCNQ, however, mutations in sei also cause extensive structural remodeling of the myofibrillar organization, which suggests that hERG channel function has a novel link to sarcomeric and myofibrillar integrity. We conclude that deficiency of ion channels with similar electrical functions in cardiomyocytes can lead to different types or extents of electrical and/or structural remodeling impacting cardiac output.
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