Evidence map›Paper›PMID 39950024›Full record

ArticleFrontiers in endocrinology2025

Role of glucocorticoid receptor expression in Chronic Chagas Cardiomyopathy: implications for inflammation and cardiac hypertrophy.

Florencia B González, Antonella Pacini, Araceli Castro, Susana Lioi, Silvina R Villar, Luciano D'Attilio, Rodolfo D Leiva, Liliana Favaloro, Oscar A Bottasso, Carlos A Vigliano and 1 more

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Florencia B GonzálezInstituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET), Rosario, Argentina.
Antonella PaciniInstituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET), Rosario, Argentina.
Araceli CastroInstituto de Medicina Traslacional, Trasplante y Bioingeniería (IMeTTyB), Universidad Favaloro-CONICET, Buenos Aires, Argentina.
Susana LioiLaboratorio Central del Hospital Provincial del Centenario, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Rosario, Argentina.
Silvina R VillarInstituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET), Rosario, Argentina.
Luciano D'AttilioInstituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET), Rosario, Argentina.
Rodolfo D LeivaFacultad de Ciencias Médicas, Universidad Nacional de Rosario, Rosario, Argentina.
Liliana FavaloroServicio de Insuficiencia Cardíaca y Trasplante Cardíaco, Hospital Universitario Fundación Favaloro, Buenos Aires, Argentina.
Oscar A BottassoInstituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET), Rosario, Argentina.
Carlos A ViglianoInstituto de Medicina Traslacional, Trasplante y Bioingeniería (IMeTTyB), Universidad Favaloro-CONICET, Buenos Aires, Argentina.
Ana Rosa PérezInstituto de Inmunología Clínica y Experimental de Rosario (IDICER-CONICET), Rosario, Argentina.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Chronic Chagasic Cardiomyopathy (CCC) has an infectious and inflammatory nature. Recent data also suggest an association with altered regulation of glucocorticoid (GC)-mediated circuits failing to control systemic inflammation. However, the involvement of glucocorticoid receptors (GR) and their isoforms have been unexplored. Materials and methods: The expression of GR-α/β isoforms, 11β-hydroxysteroid dehydrogenase type-1 (11β-HSD1), inflammatory cytokines, and the GC-regulated gene tristetraprolin (TTP) in peripheral blood mononuclear cells (PBMCs) as well as GR immunoreactivity in the myocardium from CCC individuals were evaluated by qPCR and immunohistochemistry respectively. Heart control samples with no evidence of structural heart disease and from ischemic cardiomyopathy patients were included. The presence of inflammatory infiltrates and fibrosis were also recorded. Results: GR-α was expressed similarly in the PBMCs from Co and CCC individuals, but 11β-HSD1 expression was increased only in CCC, conjointly with enhanced ratios of IL-6/TTP and IFN-γ/TTP. In the inflamed myocardium from CCC patients, positive GR expression correlated with the intensity of the inflammatory infiltrate and cardiac hypertrophy. Conclusion: The infectious and inflammatory nature of CCC pathology seems strongly connected with the expression of GR in cardiac tissue samples, providing a stimulating background for further studies addressed to elucidate the influence of GR expression and function on CCC pathophysiology and cardiomyocyte hypertrophy.

Indexed as

CardiomegalyChagas CardiomyopathyInflammationReceptors, Glucocorticoid11-beta-Hydroxysteroid Dehydrogenase Type 1AdultAgedChronic DiseaseFemaleHumansLeukocytes, MononuclearMaleMiddle AgedMyocardium11-beta-Hydroxysteroid Dehydrogenase Type 1glucocorticoid receptor alphaReceptors, Glucocorticoid11β-hydroxysteroid dehydrogenase type 1cardiomyocytechronic chagasic cardiomyopathyglucocorticoid receptorhypertrophyischemic cardiomyopathy

Identifiers

PMID39950024
PMCPMC11821487

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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.