Evidence map›Paper›PMID 40201591›Full record

ArticleEuropean heart journal open2025

Inhibiting atrial natriuretic peptide clearance reduces myocardial fibrosis and improves cardiac function in diabetic rats.

Jules Joel Bakhos, Youakim Saliba, Joelle Hajal, Guy Achkouty, Hrag Oskaridjian, Miguel Albuquerque, Chloé Azevedo, Albert Semaan, Nadine Suffee, Elise Balse and 2 more

Abstract read
In one paragraph

Article in European heart journal open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

12 authors.

Jules Joel BakhosLaboratory of Research in Physiology and Pathophysiology, Faculty of Medicine, Saint-Joseph University of Beirut, 17-5208 - Mar Mikhaël, Beirut 1104 2020, Lebanon.
Youakim SalibaLaboratory of Research in Physiology and Pathophysiology, Faculty of Medicine, Saint-Joseph University of Beirut, 17-5208 - Mar Mikhaël, Beirut 1104 2020, Lebanon.
Joelle HajalLaboratory of Research in Physiology and Pathophysiology, Faculty of Medicine, Saint-Joseph University of Beirut, 17-5208 - Mar Mikhaël, Beirut 1104 2020, Lebanon.
Guy AchkoutyLaboratory of Research in Physiology and Pathophysiology, Faculty of Medicine, Saint-Joseph University of Beirut, 17-5208 - Mar Mikhaël, Beirut 1104 2020, Lebanon.
Hrag OskaridjianLaboratory of Research in Physiology and Pathophysiology, Faculty of Medicine, Saint-Joseph University of Beirut, 17-5208 - Mar Mikhaël, Beirut 1104 2020, Lebanon.
Miguel AlbuquerqueINSERM, Centre de Recherche sur L'inflammation, UMR 1149, Université Paris-Cité, 45 Rue des Saints-Pères 75006 Paris, France.
Chloé AzevedoInstitute of Cardiometabolism and Nutrition, IHU ICAN, Sorbonne University, INSERM UMR_S1166 Pitié-Salpêtrière Hospital, 47-83 boulevard de l'Hôpital, 75013 Paris, France.
Albert SemaanLaboratory of Research in Physiology and Pathophysiology, Faculty of Medicine, Saint-Joseph University of Beirut, 17-5208 - Mar Mikhaël, Beirut 1104 2020, Lebanon.
Nadine SuffeeInstitute of Cardiometabolism and Nutrition, IHU ICAN, Sorbonne University, INSERM UMR_S1166 Pitié-Salpêtrière Hospital, 47-83 boulevard de l'Hôpital, 75013 Paris, France.
Elise BalseInstitute of Cardiometabolism and Nutrition, IHU ICAN, Sorbonne University, INSERM UMR_S1166 Pitié-Salpêtrière Hospital, 47-83 boulevard de l'Hôpital, 75013 Paris, France.
Stéphane N HatemInstitute of Cardiometabolism and Nutrition, IHU ICAN, Sorbonne University, INSERM UMR_S1166 Pitié-Salpêtrière Hospital, 47-83 boulevard de l'Hôpital, 75013 Paris, France.
Nassim FaresLaboratory of Research in Physiology and Pathophysiology, Faculty of Medicine, Saint-Joseph University of Beirut, 17-5208 - Mar Mikhaël, Beirut 1104 2020, Lebanon.ORCID https://orcid.org/0000-0002-2935-2611

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims: Natriuretic peptides (NPs) exert pleiotropic effects through the recruitment of cyclic guanosine monophosphate (cGMP) signalling pathways depending on their bioavailability, which is regulated by clearance receptors and peptidases. Here, we tested the hypothesis that increasing myocardial bioavailability of NP has a beneficial effect on heart failure. We studied the effects of a mutated NP, M-atrial natriuretic peptide (MANP), resistant to neprilysin in a model of diabetic cardiomyopathy characterized by marked myocardial fibrosis. Methods and results: Natriuretic peptides as well as sacubitril were delivered via osmotic mini-pumps to high-fat/streptozotocin-induced Type 2 diabetic (T2D) rats. Cardiac function was evaluated by echocardiography. Myocardial remodelling was studied by histological approaches, collagen phenotype, and atrial natriuretic peptide (ANP)/cGMP concentrations. Live-cell cGMP biosensing was conducted on cultured rat cardiac fibroblasts to investigate the biological effects of NP. Cyclic guanosine monophosphate signalling pathway was studied using multiple antibody arrays and biochemical assays in cardiac tissue and cultured fibroblasts. M-atrial natriuretic peptide exhibits superior efficacy than ANP in reducing left ventricular dysfunction and myocardial fibrosis with less extracellular matrix deposition. Conclusion: Myocardial bioavailability of ANP is a major determinant of peptide efficacy in reducing cardiac fibrosis and improving pump function during diabetic cardiomyopathy.

Indexed as

Cardiac fibrosisCardiomyopathycGMP/PKGDiabetesMutated atrial natriuretic peptide

Identifiers

PMID40201591
PMCPMC11977460

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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.