ArticlebioRxiv : the preprint server for biology2025
Interferon signaling promotes early neutrophil recruitment after zebrafish heart injury.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Heart injury triggers a robust cellular response in zebrafish, characterized by neovascularization, immune cell activation, and the infiltration of proliferative cardiomyocytes that collectively lead to scarless regeneration. Upon injury, damage-associated molecular patterns are released by dying cells and injured extracellular matrix. These molecules bind to pattern recognition receptors on various cell types, promoting inflammation and immune cell recruitment by upregulating chemokines and pro-inflammatory cytokines. We previously identified the activation of injury-induced interferon signaling as a distinguishing feature between the regenerative zebrafish and non-regenerative medaka. Here, we establish interferon-Φ1 (IFN 1) as the primary driver of interferon signaling after zebrafish heart injury. IFN 1 expression is induced hours after injury and directs interferon-stimulated gene expression, which peaks at 72 hours post-injury. This response is lost in
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