Evidence map›Paper›PMID 32131460›Full record

ReviewCells2020

Exosomes: From Potential Culprits to New Therapeutic Promise in the Setting of Cardiac Fibrosis.

Roman Tikhomirov, Benedict Reilly-O' Donnell, Francesco Catapano, Giuseppe Faggian, Julia Gorelik, Fabio Martelli, Costanza Emanueli

Abstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–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

38 citing papers in PubMed.

  1. Trial
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  3. Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
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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

7 authors.

Roman TikhomirovNational Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.
Benedict Reilly-O' DonnellNational Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.
Francesco CatapanoNational Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.
Giuseppe FaggianDepartment of Surgery, Dentistry, Pediatrics and Gynecology, Cardiovascular Science, The University of Verona, Policlinico G.B. Rossi, P.le. La Scuro 10, 37134 Verona, Italy.ORCID 0000-0001-5371-5761
Julia GorelikNational Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.ORCID 0000-0002-6586-0170
Fabio MartelliDepartment of Surgery, Dentistry, Pediatrics and Gynecology, Cardiovascular Science, The University of Verona, Policlinico G.B. Rossi, P.le. La Scuro 10, 37134 Verona, Italy.ORCID 0000-0002-8624-7738
Costanza EmanueliNational Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.

Funding

British Heart Foundation CH/15/1/31199British Heart Foundation RG/15/5/31446British Heart Foundation RG/17/13/33173British Heart Foundation RG/20/9/35101
6 · The paper itself

Abstract

Fibrosis is a significant global health problem associated with many inflammatory and degenerative diseases affecting multiple organs, individually or simultaneously. Fibrosis develops when extracellular matrix (ECM) remodeling becomes excessive or uncontrolled and is associated with nearly all forms of heart disease. Cardiac fibroblasts and myofibroblasts are the main effectors of ECM deposition and scar formation. The heart is a complex multicellular organ, where the various resident cell types communicate between themselves and with cells of the blood and immune systems. Exosomes, which are small extracellular vesicles, (EVs), contribute to cell-to-cell communication and their pathophysiological relevance and therapeutic potential is emerging. Here, we will critically review the role of endogenous exosomes as possible fibrosis mediators and discuss the possibility of using stem cell-derived and/or engineered exosomes as anti-fibrotic agents.

Indexed as

ExosomesFibroblastsFibrosisHeartHeart FailureHumanscardiac fibrosisEVs engineeringexosomesextracellular vesicle (EVs)heart failuremicroRNAsnoncoding RNAsstem cells

Identifiers

PMID32131460
PMCPMC7140485

What OpenQuestion holds

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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.