Evidence map›Paper›PMID 33804308›Full record

ReviewMedical sciences (Basel, Switzerland)2021

Fibrosis after Myocardial Infarction: An Overview on Cellular Processes, Molecular Pathways, Clinical Evaluation and Prognostic Value.

Renato Francesco Maria Scalise, Rosalba De Sarro, Alessandro Caracciolo, Rita Lauro, Francesco Squadrito, Scipione Carerj, Alessandra Bitto, Antonio Micari, Gianluca Di Bella, Francesco Costa and 1 more

Abstract readReview
In one paragraph

Review in Medical sciences (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

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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

11 authors.

Renato Francesco Maria ScaliseDepartment of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.ORCID 0000-0001-9149-0217
Rosalba De SarroDepartment of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.
Alessandro CaraccioloDepartment of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.
Rita LauroSection of Pharmacology, Department of Clinical and Experimental Medicine, University of Messina, 98100 Messina, Italy.
Francesco SquadritoSection of Pharmacology, Department of Clinical and Experimental Medicine, University of Messina, 98100 Messina, Italy.ORCID 0000-0002-8868-0762
Scipione CarerjDepartment of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.
Alessandra BittoSection of Pharmacology, Department of Clinical and Experimental Medicine, University of Messina, 98100 Messina, Italy.
Antonio MicariDepartment of Biomedical and Dental Sciences and Morphological and Functional Imaging, University of Messina, A.O.U. Policlinico "G. Martino", 98100 Messina, Italy.
Gianluca Di BellaDepartment of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.
Francesco CostaDepartment of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.ORCID 0000-0002-3097-2834
Natasha IrreraDepartment of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ischemic injury caused by myocardial infarction activates a complex healing process wherein a powerful inflammatory response and a reparative phase follow and balance each other. An intricate network of mediators finely orchestrate a large variety of cellular subtypes throughout molecular signaling pathways that determine the intensity and duration of each phase. At the end of this process, the necrotic tissue is replaced with a fibrotic scar whose quality strictly depends on the delicate balance resulting from the interaction between multiple actors involved in fibrogenesis. An inflammatory or reparative dysregulation, both in term of excess and deficiency, may cause ventricular dysfunction and life-threatening arrhythmias that heavily affect clinical outcome. This review discusses cellular process and molecular signaling pathways that determine fibrosis and the imaging technique that can characterize the clinical impact of this process in-vivo.

Indexed as

Myocardial InfarctionCicatrixFibrosisHumansPrognosisWound Healingcardiac magnetic resonancefibrosisinflammationmolecular pathwaysmyocardial infarctionprognostic value

Identifiers

PMID33804308
PMCPMC7931027

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.