Overview
- Researchers report that a neutrophil-intrinsic circadian program governs inflammatory damage, with daytime heart attacks causing more tissue injury than nighttime events.
- Analysis of records from 2,043 myocardial infarction patients linked higher admission neutrophil counts to greater cardiac injury and altered day–night patterns in severity.
- Neutrophil-specific disruption of the clock gene Bmal1 in mice diminished overall myocardial damage and erased diurnal spikes, implicating neutrophil timing as causal.
- Oscillations in CXCL12 signaling through CXCR4 functioned as a protective checkpoint; genetic and pharmacologic CXCR4 activation induced a night-like, less damaging neutrophil state.
- The experimental CXCR4 agonist ATI2341 reduced vascular and cardiac injury, repositioned neutrophils to the injury core, preserved host defense, and slightly improved control of Staphylococcus aureus, indicating preclinical therapeutic potential that now requires clinical trials.