Persistent interferon-gamma fuels chronic cardiac remodeling after heart attacks in aged mice
A conserved interferon-gamma signature and heightened T cell recruitment drive worse long-term heart failure outcomes in older mice following myocardial infarction.
Researchers compared post-myocardial infarction inflammatory responses in 2-month-old and 18-month-old C57BL/6 J mice of both sexes. They tracked interferon-gamma-producing cells using Ifng-YFP reporter mice and identified an interferon-gamma production signature that is conserved across mouse and human physiological aging. Following myocardial infarction, the aged mouse heart displayed an increased pro-inflammatory gene expression signature along with enhanced recruitment of interferon-gamma-expressing T cells. While this age-associated inflammation showed minimal impact during acute post-infarction responses, a persistent interferon-gamma signature in elderly mice was associated with aggravated chronic adverse cardiac remodeling. The authors conclude that age-related smoldering inflammation may fuel the long-term progression of ischemic heart failure.
Why it matters
The findings clarify how age-related immune alterations impede tissue repair after injury. They suggest that persistent, smoldering inflammation rather than the initial acute response drives post-infarction heart failure in older organisms.
Caveats
The primary mechanistic and post-infarction findings were established in mice, and the abstract does not provide details on sample sizes or the human data used to demonstrate the conserved signature.
- Altered intercellular communication
- Chronic inflammation
- Type I interferon signalling
- IFNG
- Ischemic cardiomyopathy
- Myocardial infarction
- IFN-γ
- Homo sapiens
- Mus musculus
The paper
Immune responses following myocardial infarction in aged mice
Melika ET, Ashour D, Appel M et al.
Journal of Molecular and Cellular Cardiology · 28 Sep 2026