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A cardiovascular dynamic analysis in zebrafish embryos reveals trifloxystrobin-induced cardiovascular dysfunction
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DOI：10.1016/j.cbpc.2026.110636.png)
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Abstract
En 中文
• TFX induces bioenergetic impairment, leading to growth retardation and nutrient retention. • Valve insufficiency compromises circulation despite compensatory myocardial hyper-contractility. • Downregulation of the mechanosensitive klf2a drives valve defects and severe blood regurgitation. • Standard volumetric methods overestimate cardiac output; a regurgitation analysis is critical for accuracy. • Sublethal TFX triggers pathological cardiac remodeling and threatens fish fitness.
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