Evidence map›Paper›PMID 36221014›Full record

ReviewHeart failure reviews2023

Treatment of cardiac fibrosis: from neuro-hormonal inhibitors to CAR-T cell therapy.

Paolo Morfino, Alberto Aimo, Vincenzo Castiglione, Carolina Gálvez-Montón, Michele Emdin, Antoni Bayes-Genis

Open access · hybridAbstract readReview
In one paragraph

Review in Heart failure reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Microstructural disease and hypoperfusion in dilated cardiomyopathy underpin midwall septal fibrosis.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2026
    Article
  5. Review
  6. Engineering Immune Cell to Counteract Aging and Aging-Associated Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Observational
  15. Article
  16. CAR T-Cell Therapy for Rheumatic Diseases: What Does the Future Hold?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  17. Review
  18. Nanomedicine for Diagnosis and Treatment of Cardiac Fibrosis.International journal of nanomedicine · 2025
    Review
  19. Review
  20. Article
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

6 authors at 3 institutions in 2 countries.

Paolo MorfinoInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Alberto AimoInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy. a.aimo@santannapisa.it.ORCID 0000-0001-9129-9519
Vincenzo CastiglioneInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Carolina Gálvez-MontónInstitut del Cor, Hospital Universitari Germans Trias I Pujol, Badalona, Spain.
Michele EmdinInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Antoni Bayes-GenisInstitut del Cor, Hospital Universitari Germans Trias I Pujol, Badalona, Spain.
Scuola Superiore Sant'Anna · ITInstituto de Salud Carlos III · ESUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibrosis is characterized by the deposition of extracellular matrix proteins in the spaces between cardiomyocytes following both acute and chronic tissue damage events, resulting in the remodeling and stiffening of heart tissue. Fibrosis plays an important role in the pathogenesis of many cardiovascular disorders, including heart failure and myocardial infarction. Several studies have identified fibroblasts, which are induced to differentiate into myofibroblasts in response to various types of damage, as the most important cell types involved in the fibrotic process. Some drugs, such as inhibitors of the renin-angiotensin-aldosterone system, have been shown to be effective in reducing cardiac fibrosis. There are currently no drugs with primarily anti-fibrotic action approved for clinical use, as well as the evidence of a clinical efficacy of these drugs is extremely limited, despite the numerous encouraging results from experimental studies. A new approach is represented by the use of CAR-T cells engineered in vivo using lipid nanoparticles containing mRNA coding for a receptor directed against the FAP protein, expressed by cardiac myofibroblasts. This strategy has proved to be safe and effective in reducing myocardial fibrosis and improving cardiac function in mouse models of cardiac fibrosis. Clinical studies are required to test this novel approach in humans.

Indexed as

Myocardial InfarctionReceptors, Chimeric AntigenAnimalsCell- and Tissue-Based TherapyFibroblastsFibrosisHumansMiceMyocardiumMyocytes, CardiacReceptors, Chimeric AntigenAnti-fibrotic therapiesCAR-T cellsFibrosisHeart failureMyocardium

Identifiers

PMID36221014
PMCPMC9553301
OpenAlexW4304471552

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.