ArticleCirculation2021
Isolevuglandin-Modified Cardiac Proteins Drive CD4+ T-Cell Activation in the Heart and Promote Cardiac Dysfunction.
Article in Circulation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 66 citations in OpenAlex.
- Heart-specific T cell responses: from antigens to disease mechanisms.Nature reviews. Cardiology · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts.Journal of the American Heart Association · 2026Article
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Endothelial Cell Stimulator of Interferon Genes Regulates IL-6 Production and Is Required for Pathologic Cardiac Hypertrophy and Contractile Dysfunction in Experimental Heart Failure.The American journal of pathology · 2025Article
- Salt sensitivity of blood pressure: mechanisms and sex-specific differences.Nature reviews. Cardiology · 2025Review
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- Assessment of pit viper associated subclinical myocardial injury by speckle tracking imaging.Scientific reports · 2025Article
- IL-22 Attenuates Pressure Overload-Induced Heart Failure and Inflammation.Journal of cardiovascular translational research · 2025Article
- Experimental pressure overload induces a cardiac neoantigen specific humoral immune response.Journal of molecular and cellular cardiology · 2025Article
- Pathophysiology of Group 3 Pulmonary Hypertension Associated with Lung Diseases and/or Hypoxia.International journal of molecular sciences · 2025Review
- T cells in cardiac health and disease.The Journal of clinical investigation · 2025Review
- Autoimmune-Like Mechanism in Heart Failure Enables Preventive Vaccine Therapy.Circulation research · 2025Article
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Metabolic pathways for removing reactive aldehydes are diminished in the skeletal muscle during heart failure.Skeletal muscle · 2024Article
- Posttranslationally modified self-peptides promote hypertension in mouse models.The Journal of clinical investigation · 2024Article
- Cytotoxic T cells drive doxorubicin-induced cardiac fibrosis and systolic dysfunction.Nature cardiovascular research · 2024Article
- Immune Mechanisms in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024Review
- LNK/SH2B3 loss of function increases susceptibility to murine and human atrial fibrillation.Cardiovascular research · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundDespite the well-established association between T-cell-mediated inflammation and nonischemic heart failure, the specific mechanisms triggering T-cell activation during the progression of heart failure and the antigens involved are poorly understood. We hypothesized that myocardial oxidative stress induces the formation of isolevuglandin (IsoLG)-modified proteins that function as cardiac neoantigens to elicit CD4+ T-cell receptor (TCR) activation and promote heart failure.
methodsWe used transverse aortic constriction in mice to trigger myocardial oxidative stress and T-cell infiltration. We profiled the TCR repertoire by mRNA sequencing of intramyocardial activated CD4+ T cells in Nur77
resultsWe discovered that TCR antigen recognition increases in the left ventricle as cardiac dysfunction progresses and identified a limited repertoire of activated CD4+ T-cell clonotypes in the left ventricle. Antigen presentation of endogenous antigens was required to develop cardiac dysfunction because
conclusionsOur study demonstrates an important role of reactive oxygen species-induced formation of IsoLG-modified cardiac neoantigens that lead to TCR-dependent CD4+ T-cell activation within the heart.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.