Evidence map›Paper›PMID 38982146›Full record

ReviewNature reviews. Cancer2024

Immune-checkpoint inhibitor-mediated myocarditis: CTLA4, PD1 and LAG3 in the heart.

Amir Z Munir, Alan Gutierrez, Juan Qin, Andrew H Lichtman, Javid J Moslehi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

62 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Cell death: immunogenic potential of cuproptosis in cancer.Signal transduction and targeted therapy · 2026
    Article
  7. Article
  8. Article
  9. Article
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  12. Post-viral myocarditis.Heart failure reviews · 2026
    Review
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  18. Article
  19. Article
  20. Article

2 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

5 authors.

Amir Z Munir *Section of Cardio-Oncology & Immunology, Cardiovascular Research Institute (CVRI), University of California San Francisco, School of Medicine, San Francisco, CA, USA.ORCID http://orcid.org/0009-0009-3512-5851
Alan Gutierrez *Section of Cardio-Oncology & Immunology, Cardiovascular Research Institute (CVRI), University of California San Francisco, School of Medicine, San Francisco, CA, USA.
Juan QinSection of Cardio-Oncology & Immunology, Cardiovascular Research Institute (CVRI), University of California San Francisco, School of Medicine, San Francisco, CA, USA.
Andrew H LichtmanDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Javid J MoslehiSection of Cardio-Oncology & Immunology, Cardiovascular Research Institute (CVRI), University of California San Francisco, School of Medicine, San Francisco, CA, USA. Javid.moslehi@ucsf.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune-checkpoint inhibitors (ICIs) have revolutionized oncology, with nearly 50% of all patients with cancer eligible for treatment with ICIs. However, patients on ICI therapy are at risk for immune-related toxicities that can affect any organ. Inflammation of the heart muscle, known as myocarditis, resulting from ICI targeting cytotoxic T lymphocyte-associated antigen 4 (CTLA4), programmed cell death protein 1 (PD1) and PD1 ligand 1 (PDL1) is an infrequent but potentially fatal complication. ICI-mediated myocarditis (ICI-myocarditis) is a growing clinical entity given the widespread use of ICIs, its increased clinical recognition and growing use of combination ICI treatment, a well-documented risk factor for ICI-myocarditis. In this Review, we approach ICI-myocarditis from a basic and mechanistic perspective, synthesizing the recent data from both preclinical models and patient samples. We posit that mechanistic understanding of the fundamental biology of immune-checkpoint molecules may yield new insights into disease processes, which will enable improvement in diagnostic and therapeutic approaches. The syndrome of ICI-myocarditis is novel, and our understanding of immune checkpoints in the heart is in its nascency. Yet, investigations into the pathophysiology will inform better patient risk stratification, improved diagnostics and precision-based therapies for patients.

Indexed as

CTLA-4 AntigenImmune Checkpoint InhibitorsLymphocyte Activation Gene 3 ProteinMyocarditisProgrammed Cell Death 1 ReceptorAnimalsAntigens, CDHumansNeoplasmsAntigens, CDCTLA-4 AntigenCTLA4 protein, humanImmune Checkpoint InhibitorsLag3 protein, humanLymphocyte Activation Gene 3 ProteinPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

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.