Myocardial inflammation comes of age
Abstract
Life expectancy has steadily increased over the past century, as has the occurrence of age-related diseases, most notably myocardial diseases. Aging is often accompanied by increased low-grade chronic inflammation, accumulation of terminally differentiated T-cells poised with proinflammatory phenotypes, and clonal hematopoiesis. These systemic alterations have been consistently shown to impact myocardial physiology, individual susceptibility to heart diseases and long-term heart disease prognosis. In recent years, progress has been made in understanding the interindividual (cross-sectional) and intraindividual (longitudinal) variability in the global immunosenescence profile, and novel immune-aging metric-based scoring systems bearing potential to predict cardiovascular events have emerged. We herein suggest that monitoring the patients’ individual immunosenescence trajectories, in addition to the classic cardiological work-up, could provide valuable diagnostic/prognostic information. Similarly, we propose that basic research in cardio-immunology could attain a deeper mechanistic understanding of age-related diseases and a more meaningful translational impact if the ‘aging context’ was embraced more systematically.
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BibTeX
@article{appel2026myocardial,
title = {{Myocardial inflammation comes of age}},
author = {Marc Appel and Stefan Frantz and Gustavo Campos Ramos},
journal = {Current Opinion in Physiology},
year = {2026},
month = oct,
doi = {10.1016/j.cophys.2020.09.006},
url = {https://hal.science/hal-05780796v1},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Myocardial inflammation comes of age
AU - Marc Appel
AU - Stefan Frantz
AU - Gustavo Campos Ramos
PY - 2026
DA - 2026/10/06
JO - Current Opinion in Physiology
DO - 10.1016/j.cophys.2020.09.006
UR - https://hal.science/hal-05780796v1
AB - Life expectancy has steadily increased over the past century, as has the occurrence of age-related diseases, most notably myocardial diseases. Aging is often accompanied by increased low-grade chronic inflammation, accumulation of terminally differentiated T-cells poised with proinflammatory phenotypes, and clonal hematopoiesis. These systemic alterations have been consistently shown to impact myocardial physiology, individual susceptibility to heart diseases and long-term heart disease prognosis. In recent years, progress has been made in understanding the interindividual (cross-sectional) and intraindividual (longitudinal) variability in the global immunosenescence profile, and novel immune-aging metric-based scoring systems bearing potential to predict cardiovascular events have emerged. We herein suggest that monitoring the patients’ individual immunosenescence trajectories, in addition to the classic cardiological work-up, could provide valuable diagnostic/prognostic information. Similarly, we propose that basic research in cardio-immunology could attain a deeper mechanistic understanding of age-related diseases and a more meaningful translational impact if the ‘aging context’ was embraced more systematically.
SN - 2468-8681
SN - 2468-8673
ER -