Evidence map›Paper›PMID 31074651›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2019

T-cell recruitment to the heart: friendly guests or unwelcome visitors?

Robert M Blanton, Francisco J Carrillo-Salinas, Pilar Alcaide

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 2 pooled it
9.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Pooled it
  2. Pooled it
  3. Cell Type-Specific Roles for BRD4 in Heart Failure.Current cardiology reports · 2026
    Review
  4. Review
  5. CXCL10 Regulates Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2026
    Article
  6. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  7. Review
  8. Review
  9. Immunometabolism in heart failure.Nature reviews. Cardiology · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Immune checkpoint inhibitor-associated myocarditis: a historical and comprehensive review.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Robert M BlantonMolecular Cardiology Research Institute, Tufts Medical Center , Boston, Massachusetts.
Francisco J Carrillo-SalinasDepartment of Immunology, Tufts University School of Medicine, Boston, Massachusetts.
Pilar AlcaideDepartment of Immunology, Tufts University School of Medicine, Boston, Massachusetts.
Tufts University · USTufts Medical Center · US

Funding

Mechanisms of T cell activation in cardiac fibrosis and non-ischemic heart failureR01HL144477 · NHLBI · TUFTS UNIVERSITY BOSTON · PI ALCAIDE ALONSO, MARIA PILAR · 2019 to 2023
$3.2M
T Cell Mediated Immune Responses as a Regulator of Heart FailureR01HL123658 · NHLBI · TUFTS UNIVERSITY BOSTON · PI ALCAIDE ALONSO, MARIA PILAR · 2014 to 2018
$2.2M
Novel Protein Kinase GI Substrates in Cardiac Remodeling and Blood Pressure ControlR01HL131831 · NHLBI · TUFTS MEDICAL CENTER · PI BLANTON, ROBERT MORRIS · 2016 to 2020
$2.1M
NHLBI NIH HHS R01 HL123658NHLBI NIH HHS R01 HL131831NHLBI NIH HHS R01 HL144477
6 · The paper itself

Abstract

Myocardial inflammation can lead to lethal acute or chronic heart failure (HF). T lymphocytes (T cells), have been reported in the inflamed heart in different etiologies of HF, and more recent studies support that different T-cell subsets play distinct roles in the heart depending on the inflammation-triggering event. T cells follow sequential steps to extravasate into tissues, but their specific recruitment to the heart is determined by several factors. These include differences in T-cell responsiveness to specific chemokines in the heart environment, as well as differences in the expression of adhesion molecules in response to distinct stimuli, which regulate T-cell recruitment to the heart and have consequences in cardiac remodeling and function. This review focuses on recent advances in our understanding of the role T cells play in the heart, including its critical role for host defense to virus and myocardial healing postischemia, and its pathogenic role in chronic ischemic and nonischemic HF. We discuss a variety of mechanisms that contribute to the inflammatory damage to the heart, as well as regulatory mechanisms that limit the magnitude of T-cell-mediated inflammation. We also highlight areas in which further research is needed to understand the role T cells play in the heart and distinguish the findings reported in experimental animal models and how they may translate to clinical observations in the human heart.

Indexed as

Chemotaxis, LeukocyteLymphocyte ActivationAnimalsCardiomyopathiesCell CommunicationCytokinesFibrosisHeart FailureHumansHypertrophy, Left VentricularInflammation MediatorsMyocardiumSignal TransductionT-LymphocytesVentricular Dysfunction, LeftVentricular Function, LeftCytokinesInflammation Mediatorsheart failureT cells

Identifiers

PMID31074651
PMCPMC6692732
OpenAlexW2944052866

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.