Heart failure & cardiomyopathies
Macrophage-specific circular RNA circHIPK2, inflammation, and fibrosis after myocardial infarction
Study context
- Population
- Murine MI model with macrophage-targeted circHIPK2 inhibition; living myocardial slices from HF patients co-cultured with human iPSC-derived macrophages
Methodological detailsin vitro, murine MI model, ex vivo human myocardial slice co-culture
- In vitro
- Murine MI model
- Ex vivo human myocardial slice co-culture
Main finding
As reported in the abstract
- circHIPK2 interacts with G3BP1 to promote stress granule formation in macrophages, initiating a downstream inflammatory cascade
- circHIPK2 inhibition suppressed inflammatory signalling and reduced pro-inflammatory cytokine secretion
- In mouse MI, macrophage-specific circHIPK2 inhibition improved cardiac function, reshaped the inflammatory environment and attenuated fibrosis progression
- Silencing circHIPK2 in human macrophages promoted beneficial cardiac healing in established HF
Original publication
Macrophage-specific circular RNA circHIPK2, inflammation, and fibrosis after myocardial infarction. Eur Heart J. Published 11 February 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →