PUBLICATION

Nr4a1 modulates inflammation and heart regeneration in zebrafish

Authors
Feng, D., Dong, Y., Song, Y., Yapundich, N., Xie, Y., Spurlock, B., Lyu, T., Kuehn, L., Qian, L., Liu, J.
ID
ZDB-PUB-250625-11
Date
2025
Source
Development (Cambridge, England) : (Journal)
Registered Authors
Liu, Jiandong
Keywords
Cardiac regeneration, Macrophage, Neutrophil, Nr4a1
Datasets
GEO:GSE276850
MeSH Terms
  • Inflammation*/genetics
  • Inflammation*/metabolism
  • Fibrosis
  • Neutrophils/metabolism
  • Zebrafish Proteins*/genetics
  • Zebrafish Proteins*/metabolism
  • Regeneration*/genetics
  • Regeneration*/physiology
  • Heart*/physiology
  • Zebrafish*/genetics
  • Zebrafish*/physiology
  • Animals
  • Nuclear Receptor Subfamily 4, Group A, Member 1*/genetics
  • Nuclear Receptor Subfamily 4, Group A, Member 1*/metabolism
PubMed
40554763 Full text @ Development
Abstract
Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration, demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair, chronic inflammation, and unresolved fibrosis could impede full regenerative recovery. In this study, we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response, disrupted neutrophil migration, delayed fibrin clearance, and ultimately impaired heart regeneration. Transcriptome-wide RNA-seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably, partial inhibition of the pro-inflammatory cytokine Tnf-α rescued heart regeneration in the nr4a1 mutants, highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury.
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