ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2021
Zebrafish heart regenerates after chemoptogenetic cardiomyocyte depletion.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 11 citations in OpenAlex.
- Zebrafish as a Versatile Model for Cardiovascular Research: Peering into the Heart of the Matter.Cells · 2025Review
- Article
- Development of a Zebrafish Larvae Model for Diabetic Heart Failure With Reduced Ejection Fraction.Korean circulation journal · 2023Article
- The multifaceted nature of endogenous cardiac regeneration.Frontiers in cardiovascular medicine · 2023Review
- Two decades of heart regeneration research: Cardiomyocyte proliferation and beyond.WIREs mechanisms of diseaseReview
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundZebrafish can regenerate adult cardiac tissue following injuries from ventricular apex amputation, cryoinjury, and cardiomyocyte genetic ablation. Here, we characterize cardiac regeneration from cardiomyocyte chemoptogenetic ablation caused by localized near-infrared excited photosensitizer-mediated reactive oxygen species (ROS) generation.
resultsExposure of transgenic adult zebrafish, Tg(myl7:fapdl5-cerulean), to di-iodinated derivative of the cell- permeable Malachite Green ester fluorogen (MG-2I) and whole-body illumination with 660 nm light resulted in cytotoxic damage to about 30% of cardiac tissue. After chemoptogenetic cardiomyocyte ablation, heart function was compromised, and macrophage infiltration was detected, but epicardial and endocardial activation response was much muted when compared to ventricular amputation. The spared cardiomyocytes underwent proliferation and restored the heart structure and function in 45-60 days after ablation.
conclusionsThis cardiomyocyte ablation system did not appear to activate the epicardium and endocardium as is noted in other cardiac injury models. This approach represents a useful model to study specifically cardiomyocyte injury, proliferation and regeneration in the absence of whole organ activation. Moreover, this system can be adapted to ablate distinct cell populations in any organ system to study their function in regeneration.
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