An interferon gamma response signature links myocardial aging and immunosenescence
Open accessAbstract
Aims: Aging entails profound immunological transformations that can impact myocardial homeostasis and predispose to heart failure. However, preclinical research in the immune-cardiology field is mostly conducted in young healthy animals, which potentially weakens its translational relevance. Herein, we sought to investigate how the aging T-cell compartment associates with changes in myocardial cell biology in aged mice. Methods and results: We phenotyped the antigen-experienced effector/memory T cells purified from heart-draining lymph nodes of 2-, 6-, 12-, and 18-month-old C57BL/6J mice using single-cell RNA/T cell receptor sequencing. Simultaneously, we profiled all non-cardiomyocyte cell subsets purified from 2- to 18-month-old hearts and integrated our data with publicly available cardiomyocyte single-cell sequencing datasets. Some of these findings were confirmed at the protein level by flow cytometry. With aging, the heart-draining lymph node and myocardial T cells underwent clonal expansion and exhibited an up-regulated pro-inflammatory transcription signature, marked by an increased interferon-γ (IFN-γ) production. In parallel, all major myocardial cell populations showed increased IFN-γ responsive signature with aging. In the aged cardiomyocytes, a stronger IFN-γ response signature was paralleled by the dampening of expression levels of transcripts related to most metabolic pathways, especially oxidative phosphorylation. Likewise, induced pluripotent stem cells-derived cardiomyocytes exposed to chronic, low grade IFN-γ treatment showed a similar inhibition of metabolic activity. Conclusions: By investigating the paired age-related alterations in the T cells found in the heart and its draining lymph nodes, we provide evidence for increased myocardial IFN-γ signaling with age, which is associated with inflammatory and metabolic shifts typically seen in heart failure.
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Accumulation of activated memory cardiac T cells in the mediastinal lymph node and myocardium is associated with myocardial aging, leading to significantly lower cardiac output.
“Another investigation demonstrated that the accumulation of activated memory cardiac T cells in the mediastinal lymph node and myocardium is associated with myocardial aging, leading to significantly lower cardiac output. 271,300,301”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [300]
The Results section on the heart-draining mediastinal lymph node reports an age-related increase in CD4 effector-memory T cells, alongside increased inflammatory signatures in cardiac tissue. The paper does not establish that activated memory T cells accumulate in the myocardium or cause significantly lower cardiac output; no cardiac-output finding was found in the indexed text. (LLM, conf=0.88)
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Self-citationIdentification of a novel myosin antigen activating CD8 + T cells in C57BL/6 micePreprint
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Interferon-gamma signs off an old heart
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Immune responses following myocardial infarction in aged mice
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Self-citation
- Authors
- Ashour, D., Rebs, S., Arampatzi, P., Saliba, A.-E., Dudek, J., Schulz, R., Hofmann, U., Frantz, S., Cochain, C., Streckfuß-Bömeke, K., & Campos Ramos, G.
- Affiliations
- Universitätsklinikum Würzburg (DE)
- University of Würzburg (DE)
- University of Alberta (CA)
- Institute of Pharmacology and Toxicology, University of Würzburg, Versbacher Str. 9 , 97078 Würzburg , Germany
- Department of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Str. 6 , 97080 Würzburg , Germany
- ORCID
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2023-05-04
- Volume
- 119
- Issue
- 14
- Pages
- 2458-2468
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC10651211
- OpenAlex
- W4368347468
- Cited by
- 39
- References
- 55
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 18 · 2023: 2
- FWCI
- 7.87
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cardiovascular Research (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- German Research Foundation (411619907, SFB1525, 453989101)
- European Research Area Network—Cardiovascular Diseases (ERANET-CVD JCT2018)
- AIR-MI Consortium (01KL1902)
- G.C.R. and C.C.
- Centre for Clinical Research Würzburg (E-354, E-353)
- Collaborative Research Centre ‘Cardio-Immune interfaces’
- Humboldt Research Award
- Alexander von Humboldt Foundation
- Canadian Institute for Health Research (143299)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- cardiac aging, immunosenescence, interferon-gamma, T cells, effector memory T cells, clonal expansion, cardiomyocyte metabolism, oxidative phosphorylation, iPSC-derived cardiomyocytes, heart failure, aged mice
- MeSH terms
- Immunosenescence, Aging, Animals, Heart Failure, Interferon-gamma, Mice, Inbred C57BL, Mice
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