Evidence map›Paper›PMID 37538375›Full record

ReviewFrontiers in physiology2023

From bedside to the bench: patient-specific hiPSC-EC models uncover endothelial dysfunction in genetic cardiomyopathies.

Martina Rabino, Elena Sommariva, Serena Zacchigna, Giulio Pompilio

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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

4 authors at 3 institutions in 1 country.

Martina RabinoUnit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino-IRCCS, Milan, Italy.
Elena SommarivaUnit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino-IRCCS, Milan, Italy.
Serena ZacchignaUnit of Cardio-Oncology, Centro Cardiologico Monzino-IRCCS, Milan, Italy.
Giulio PompilioUnit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino-IRCCS, Milan, Italy.
Centro Cardiologico Monzino · ITInternational Centre for Genetic Engineering and Biotechnology · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic cardiomyopathies are a group of inherited disorders in which myocardial structure and function are damaged. Many of these pathologies are rare and present with heterogenous phenotypes, thus personalized models are required to completely uncover their pathological mechanisms and develop valuable therapeutic strategies. Both cardiomyocytes and fibroblasts, differentiated from patient-specific human induced pluripotent stem cells, represent the most studied human cardiac cell models in the context of genetic cardiomyopathies. While endothelial dysfunction has been recognized as a possible pathogenetic mechanism, human induced pluripotent stem cell-derived endothelial cells are less studied, despite they constitute a suitable model to specifically dissect the role of the dysfunctional endothelium in the development and progression of these pathologies. In this review, we summarize the main studies in which human induced pluripotent stem cell-derived endothelial cells are used to investigate endothelial dysfunction in genetic-based cardiomyopathies to highlight new potential targets exploitable for therapeutic intervention, and we discuss novel perspectives that encourage research in this direction.

Indexed as

disease modellingendothelial dysfunction (ED)genetic cardiomyopathieshiPSC-derived endothelial cells (hiPSC-ECs)human induced pluripotent stem cells (hiPSCs)personalized medicine

Identifiers

PMID37538375
PMCPMC10394630
OpenAlexW4384827841

What OpenQuestion holds

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LicenceCC BY
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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.