Evidence map›Paper›PMID 35204091›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Unraveling and Targeting Myocardial Regeneration Deficit in Diabetes.

Claudia Molinaro, Luca Salerno, Fabiola Marino, Mariangela Scalise, Nadia Salerno, Loredana Pagano, Antonella De Angelis, Eleonora Cianflone, Daniele Torella, Konrad Urbanek

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

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  14. Polarizing Macrophage Functional Phenotype to Foster Cardiac Regeneration.International journal of molecular sciences · 2023
    Review
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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

10 authors at 2 institutions in 1 country.

Claudia MolinaroDepartment of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Luca SalernoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Fabiola MarinoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0001-9043-6032
Mariangela ScaliseDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Nadia SalernoDepartment of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Loredana PaganoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Antonella De AngelisDepartment of Experimental Medicine, University of Campania "L. Vanvitelli", 80138 Naples, Italy.
Eleonora CianfloneDepartment of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Daniele TorellaDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Konrad UrbanekDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy.
Magna Graecia University · ITUniversity of Campania "Luigi Vanvitelli" · IT

Funding

Ministry of Education, University and 380 Research PON03PE00009_2-iCAREMinistry of Education, University and Research PRIN2017 2017NKB2N4_005
6 · The paper itself

Abstract

Cardiomyopathy is a common complication in diabetic patients. Ventricular dysfunction without coronary atherosclerosis and hypertension is driven by hyperglycemia, hyperinsulinemia and impaired insulin signaling. Cardiomyocyte death, hypertrophy, fibrosis, and cell signaling defects underlie cardiomyopathy. Notably, detrimental effects of the diabetic milieu are not limited to cardiomyocytes and vascular cells. The diabetic heart acquires a senescent phenotype and also suffers from altered cellular homeostasis and the insufficient replacement of dying cells. Chronic inflammation, oxidative stress, and metabolic dysregulation damage the population of endogenous cardiac stem cells, which contribute to myocardial cell turnover and repair after injury. Therefore, deficient myocardial repair and the progressive senescence and dysfunction of stem cells in the diabetic heart can represent potential therapeutic targets. While our knowledge of the effects of diabetes on stem cells is growing, several strategies to preserve, activate or restore cardiac stem cell compartments await to be tested in diabetic cardiomyopathy.

Indexed as

adult stem cellscardiac stem cellsdiabetes mellitusdiabetic cardiomyopathysenescence

Identifiers

PMID35204091
PMCPMC8868283
OpenAlexW4214717735

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.