Authors
Ebram Tharwat Melika, DiyaaElDin Ashour, Marc Appel, Daphne Steder, Panagiota Arampatzi, Thorsten Bischler, Lisa Popiolkowski, Ulrich Hofmann, Stefan Frantz, Gustavo Campos Ramos
Published in
Journal of molecular and cellular cardiology. Sep 28, 2026. Epub Sep 28, 2026.
Abstract
Aging is a major risk factor for cardiovascular diseases and is often accompanied by systemic alterations of the immune system, such as the accumulation of terminally differentiated T cells, clonal hematopoiesis of intermediate potential, and dysregulated production of pro-inflammatory cytokines. However, how the aging immune system impacts post-myocardial infarction (MI) repair remains poorly understood. In the present study, we compared the post-MI inflammatory responses in 2- and 18-month-old C57BL/6 J mice of both sexes and monitored the distribution of interferon-gamma (IFN-γ) producing cells in these conditions using Ifng-YFP reporter mice. Our results show a conserved IFN-γ production signature both in mice and humans during physiological aging. In mice, the aging myocardium exhibited increased pro-inflammatory gene expression signature with increased recruitment of IFN-γ-expressing T cells following MI. Moreover, while this age-related inflammation had little impact in the acute post-MI responses, a persistent IFN-γ-production signature observed in elderly mice was associated with an aggravation of chronic adverse cardiac remodeling. Taken together, our results indicate that age-related smoldering inflammation may fuel the long-term progression of ischemic heart failure.
PMID:
42805582
Bibliographic data and abstract were imported from PubMed on 29 Sep 2026.
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