Evidence map›Paper›PMID 32575374›Full record

ReviewInternational journal of molecular sciences2020

Modeling Cardiac Disease Mechanisms Using Induced Pluripotent Stem Cell-Derived Cardiomyocytes: Progress, Promises and Challenges.

Elvira Immacolata Parrotta, Valeria Lucchino, Luana Scaramuzzino, Stefania Scalise, Giovanni Cuda

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Elvira Immacolata ParrottaDepartment of Experimental and Clinical Medicine, Research Center for Advanced Biochemistry and Molecular Biology, University "Magna Graecia" of Catanzaro, 88100 Loc. Germaneto, Catanzaro, Italy.ORCID 0000-0001-8145-3623
Valeria LucchinoDepartment of Experimental and Clinical Medicine, Research Center for Advanced Biochemistry and Molecular Biology, University "Magna Graecia" of Catanzaro, 88100 Loc. Germaneto, Catanzaro, Italy.ORCID 0000-0002-7350-3835
Luana ScaramuzzinoDepartment of Experimental and Clinical Medicine, Research Center for Advanced Biochemistry and Molecular Biology, University "Magna Graecia" of Catanzaro, 88100 Loc. Germaneto, Catanzaro, Italy.
Stefania ScaliseDepartment of Experimental and Clinical Medicine, Research Center for Advanced Biochemistry and Molecular Biology, University "Magna Graecia" of Catanzaro, 88100 Loc. Germaneto, Catanzaro, Italy.ORCID 0000-0001-6979-1486
Giovanni CudaDepartment of Experimental and Clinical Medicine, Research Center for Advanced Biochemistry and Molecular Biology, University "Magna Graecia" of Catanzaro, 88100 Loc. Germaneto, Catanzaro, Italy.ORCID 0000-0001-6313-1866
Magna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases (CVDs) are a class of disorders affecting the heart or blood vessels. Despite progress in clinical research and therapy, CVDs still represent the leading cause of mortality and morbidity worldwide. The hallmarks of cardiac diseases include heart dysfunction and cardiomyocyte death, inflammation, fibrosis, scar tissue, hyperplasia, hypertrophy, and abnormal ventricular remodeling. The loss of cardiomyocytes is an irreversible process that leads to fibrosis and scar formation, which, in turn, induce heart failure with progressive and dramatic consequences. Both genetic and environmental factors pathologically contribute to the development of CVDs, but the precise causes that trigger cardiac diseases and their progression are still largely unknown. The lack of reliable human model systems for such diseases has hampered the unraveling of the underlying molecular mechanisms and cellular processes involved in heart diseases at their initial stage and during their progression. Over the past decade, significant scientific advances in the field of stem cell biology have literally revolutionized the study of human disease in vitro. Remarkably, the possibility to generate disease-relevant cell types from induced pluripotent stem cells (iPSCs) has developed into an unprecedented and powerful opportunity to achieve the long-standing ambition to investigate human diseases at a cellular level, uncovering their molecular mechanisms, and finally to translate bench discoveries into potential new therapeutic strategies. This review provides an update on previous and current research in the field of iPSC-driven cardiovascular disease modeling, with the aim of underlining the potential of stem-cell biology-based approaches in the elucidation of the pathophysiology of these life-threatening diseases.

Indexed as

Cell DifferentiationDisease ProgressionHeart DiseasesHumansInduced Pluripotent Stem CellsModels, BiologicalMyocytes, CardiacSignal Transductioncardiac differentiationcardiac disease modelingcardiovascular diseaseshuman induced pluripotent stem cellsiPSC-derived cardiomyocytes

Identifiers

PMID32575374
PMCPMC7352327
OpenAlexW3036591244

What OpenQuestion 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 OpenQuestion graph.