ArticleCirculation. Heart failure2015
Left Ventricular T-Cell Recruitment Contributes to the Pathogenesis of Heart Failure.
Article in Circulation. Heart failure, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
200 citing papers in PubMed, 1 synthesis or guideline pooled it, 264 citations in OpenAlex.
- Association of immune cell subsets with incident heart failure in two population-based cohorts.ESC heart failure · 2022Pooled it
- Thymopentin improves cardiac function in older patients with chronic heart failure.Anatolian journal of cardiology · 2017Trial
- Translational biology of human cardiac fibrosis.Nature cardiovascular research · 2026Review
- Heart-specific T cell responses: from antigens to disease mechanisms.Nature reviews. Cardiology · 2026Review
- Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts.Journal of the American Heart Association · 2026Article
- Single-Cell Analysis of Human Heart Failure With Preserved Ejection Fraction.Circulation research · 2026Article
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Inhibition of the programmed death protein 1 immune checkpoint and the development of heart failure in the presence of prior cardiac ischaemia.Cardiovascular research · 2026Article
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- Microvascular endothelial scavenger receptor class B type I protects against heart failure with preserved ejection fraction by inhibiting T-cell cardiotropism.EMBO molecular medicine · 2026Article
- International Utah cardiac recovery symposium (U-CARS) 2025:translational and basic science proceedings.Heart failure reviews · 2026Review
- T cell-derived IFNγ instructs ECM crosslinking by cardiac fibroblasts through LOXL3 in experimental cardiometabolic HFpEF.bioRxiv : the preprint server for biology · 2026Article
- Specific Deficiency of Naïve CD4+ T Lymphocytes Characterizes Heart Failure and Heightens Mortality Risk in the HRS.Journal of the American Heart Association · 2026Article
- CXCL10 Regulates Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2026Article
- Phenotypes and mechanisms of dysfunctional cardiac T-lymphocytes in dilated cardiomyopathy patients.Journal of molecular and cellular cardiology · 2026Article
- T Cell Polarization in Heart Failure: Any Flavor, as Long as It Is Th1.JACC. Basic to translational science · 2026Article
- Inflammation in a severe model of dystrophic cardiomyopathy contains a high proportion of T cells that contribute to onset of pathology.American journal of physiology. Heart and circulatory physiology · 2026Article
- Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment.European heart journal · 2026Review
- Interleukin-17, Interleukin-18, T Regulatory Cells, and T-Helper 17 (Th17) Cells Play a Role in Heart Failure: A Systematic Review and Meta-Analysis.Cardiology research and practice · 2026Review
- Advances in targeting myocardial fibrosis: integrating mechanisms and therapeutics.Frontiers in cardiovascular medicine · 2026Review
140 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDespite the emerging association between heart failure (HF) and inflammation, the role of T cells, major players in chronic inflammation, has only recently begun to be explored. Whether T-cell recruitment to the left ventricle (LV) participates in the development of HF requires further investigation to identify novel mechanisms that may serve for the design of alternative therapeutic interventions. METHODS AND
resultsReal-time videomicroscopy of T cells from nonischemic HF patients or from mice with HF induced by transverse aortic constriction revealed enhanced adhesion to activated vascular endothelial cells under flow conditions in vitro compared with T cells from healthy subjects or sham mice. T cells in the mediastinal lymph nodes and the intramyocardial endothelium were both activated in response to transverse aortic constriction and the kinetics of LV T-cell infiltration was directly associated with the development of systolic dysfunction. In response to transverse aortic constriction, T cell-deficient mice (T-cell receptor, TCRα(-/-)) had preserved LV systolic and diastolic function, reduced LV fibrosis, hypertrophy and inflammation, and improved survival compared with wild-type mice. Furthermore, T-cell depletion in wild-type mice after transverse aortic constriction prevented HF.
conclusionsT cells are major contributors to nonischemic HF. Their activation combined with the activation of the LV endothelium results in LV T-cell infiltration negatively contributing to HF progression through mechanisms involving cytokine release and induction of cardiac fibrosis and hypertrophy. Reduction of T-cell infiltration is thus identified as a novel translational target in HF.
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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.