Heart failure & cardiomyopathies
Novel Long Noncoding RNA HEAT4 Affects Monocyte Subtypes, Reducing Inflammation and Promoting Vascular Healing
Authors' conclusion
These results characterize a novel endogenous anti-inflammatory pathway that involves the conversion of monocyte subtypes into anti-inflammatory CD16+ monocytes.
Study context
- Population
- Patients with heart failure (HF), acute MI or cardiogenic shock; in vitro, ex vivo and mouse vascular injury models
Main finding
As reported in the abstract
- HEAT4 expression increased in blood of patients with HF, acute MI or cardiogenic shock
- HEAT4 levels distinguished patients with HF from people without HF and predicted all-cause mortality in HF cohort over 7 years
- Monocytes, particularly anti-inflammatory CD16+ monocytes, are the primary source of HEAT4 in blood
- HEAT4 transcriptionally activated by interleukin-10
- HEAT4 activates anti-inflammatory and inhibits proinflammatory gene expression; increased HEAT4 shifts toward more CD16+ monocytes
- HEAT4 binds S100A9, causing a monocyte subtype switch and reducing inflammation
- HEAT4 improves endothelial barrier integrity during inflammation and promotes vascular healing after injury in mice
Original publication
Novel Long Noncoding RNA HEAT4 Affects Monocyte Subtypes, Reducing Inflammation and Promoting Vascular Healing. Circulation. Published 15 July 2024. doi:10.
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