ArticleActa physiologica (Oxford, England)2025
Mitochondrial Dysfunction Contributes to Decompensation in a Zebrafish Model of Isoproterenol-Induced Heart Failure.
Article in Acta physiologica (Oxford, England), 2025. 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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Who cites it
5 citing papers in PubMed.
- An Anesthesia-Free Pharmacological Assay for Zebrafish Heart Failure Models Using a Microfluidic Platform.Biomedicines · 2026Article
- Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Multi-Target Cardioprotection fromAntioxidants (Basel, Switzerland) · 2026Article
- Mitochondrial Dysfunction Contributes to Decompensation in a Zebrafish Model of Isoproterenol-Induced Heart Failure.Acta physiologica (Oxford, England) · 2025Article
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7 authors.
Funding
Abstract
aimHeart failure is a clinical syndrome where the heart's structural or functional impairment leads to inadequate blood flow to meet the body's metabolic demands. Mitochondrial dysfunction is increasingly recognized as a central contributor underlying the contractile impairment observed in the failing heart. This study aimed to explore the interplay between calcium dynamics, cardiac mechanical performance, and mitochondrial ATP production during the progression of heart failure in zebrafish larvae exposed to chronic isoproterenol stimulation.
methodsHeart failure was induced by treating zebrafish larvae with 100 μM isoproterenol from 3 to 14 days postfertilization (dpf). Cardiac calcium transients, contractility, and mitochondrial ATP levels were assessed in vivo using transgenic lines expressing specific fluorescent biosensors. Additionally, transcriptomic analysis by RNA sequencing was performed on hearts collected at 14 dpf following prolonged isoproterenol exposure.
resultsAfter 4 days of isoproterenol treatment (7 dpf), larvae exhibited ventricular dilation, reduced calcium levels, and diminished contractile force (p < 0.0001), although cardiac output remained intact. In contrast, extended treatment (11 days; 14 dpf) led to decompensated heart failure, characterized by a significant decline in cardiac output (p < 0.0001). Mitochondrial ATP levels were preserved at 7 dpf but dropped markedly at 14 dpf (p < 0.0001). Transcriptomic profiling at this later stage revealed downregulation of key functions (p < 0.05) involved in mitochondrial energy metabolism and energy transfer.
conclusionIn this model, heart dysfunction was initially evidenced by cardiac dilation. At 4 days of isoproterenol treatment, calcium levels and contractility decreased. Subsequently, decompensation coincided with a collapse in mitochondrial ATP production.
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