ArticleScientific reports2015
Cardiac Optogenetics: Enhancement by All-trans-Retinal.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- A two-stage multi-scale attention-based network for weakly supervised cataract fundus image enhancement.Scientific reports · 2025Article
- Ultrathin rubbery bio-optoelectronic stimulators for untethered cardiac stimulation.Science advances · 2024Article
- Optical mapping and optogenetics in cardiac electrophysiology research and therapy: a state-of-the-art review.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024Review
- Modulating cardiac physiology in engineered heart tissue with the bidirectional optogenetic tool BiPOLES.Pflugers Archiv : European journal of physiology · 2023Article
- Cardiac optogenetics: a decade of enlightenment.Nature reviews. Cardiology · 2021Review
- Application of Fluorescence Microscopy and Behavioral Assays to Demonstrating Neuronal Connectomes and Neurotransmitter Systems inNeuromethods · 2021Article
- Feasibility of Using Adjunctive Optogenetic Technologies in Cardiomyocyte Phenotyping - from the Single Cell to the Whole Heart.Current pharmaceutical biotechnology · 2020Review
- Cardiac Optogenetics in Atrial Fibrillation: Current Challenges and Future Opportunities.BioMed research international · 2020Review
- Adeno-Associated Virus Mediated Gene Delivery: Implications for ScalableFrontiers in physiology · 2019Article
- Sub-millisecond Control of Neuronal Firing by Organic Light-Emitting Diodes.Frontiers in bioengineering and biotechnology · 2019Article
- Cardiac Optogenetics and Optical Mapping - Overcoming Spectral Congestion in All-Optical Cardiac Electrophysiology.Frontiers in physiology · 2019Review
- Review
- Cardiac Optogenetics: 2018.JACC. Clinical electrophysiology · 2018Review
- Electrophysiological Properties and Viability of Neonatal Rat Ventricular Myocyte Cultures with Inducible ChR2 Expression.Scientific reports · 2017Article
- Non-invasive phenotyping and drug testing in single cardiomyocytes or beta-cells by calcium imaging and optogenetics.PloS one · 2017Article
- Anion channelrhodopsins for inhibitory cardiac optogenetics.Scientific reports · 2016Article
- Light-based Approaches to Cardiac Arrhythmia Research: From Basic Science to Translational Applications.Clinical Medicine Insights. Cardiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
All-trans-Retinal (ATR) is a photosensitizer, serving as the chromophore for depolarizing and hyperpolarizing light-sensitive ion channels and pumps (opsins), recently employed as fast optical actuators. In mammalian optogenetic applications (in brain and heart), endogenous ATR availability is not considered a limiting factor, yet it is unclear how ATR modulation may affect the response to optical stimulation. We hypothesized that exogenous ATR may improve light responsiveness of cardiac cells modified by Channelrhodopsin2 (ChR2), hence lowering the optical pacing energy. In virally-transduced (Ad-ChR2(H134R)-eYFP) light-sensitive cardiac syncytium in vitro, ATR supplements ≤2 μM improved cardiomyocyte viability and augmented ChR2 membrane expression several-fold, while >4 μM was toxic. Employing integrated optical actuation (470 nm) and optical mapping, we found that 1-2 μM ATR dramatically reduced optical pacing energy (over 30 times) to several μW/mm(2), lowest values reported to date, but also caused action potential prolongation, minor changes in calcium transients and no change in conduction. Theoretical analysis helped explain ATR-caused reduction of optical excitation threshold in cardiomyocytes. We conclude that cardiomyocytes operate at non-saturating retinal levels, and carefully-dosed exogenous ATR can enhance the performance of ChR2 in cardiac cells and yield energy benefits over orders of magnitude for optogenetic stimulation.
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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.