Evidence map›Paper›PMID 25934765›Full record

ArticleHaematologica2015

Dietary ω-3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease.

Brian T Kalish, Alessandro Matte, Immacolata Andolfo, Achille Iolascon, Olga Weinberg, Alessandra Ghigo, James Cimino, Angela Siciliano, Emilio Hirsch, Enrica Federti and 3 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.2field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  12. Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin-1 via NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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

13 authors at 5 institutions in 2 countries.

Brian T KalishDepartment of Surgery and The Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Alessandro MatteDepartment of Medicine, University of Verona-AOUI Verona, Policlinico GB Rossi, Verona, Italy.
Immacolata AndolfoDepartment of Biochemistry, University Federico II, Naples, Italy.
Achille IolasconDepartment of Biochemistry, University Federico II, Naples, Italy.
Olga WeinbergDepartments of Pathology and Laboratory Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Alessandra GhigoMolecular Biotechnology Center and Department of Molecular Biotechology and Health Science, University of Turin, Italy.
James CiminoMolecular Biotechnology Center and Department of Molecular Biotechology and Health Science, University of Turin, Italy.
Angela SicilianoDepartment of Medicine, University of Verona-AOUI Verona, Policlinico GB Rossi, Verona, Italy.
Emilio HirschMolecular Biotechnology Center and Department of Molecular Biotechology and Health Science, University of Turin, Italy.
Enrica FedertiDepartment of Medicine, University of Verona-AOUI Verona, Policlinico GB Rossi, Verona, Italy.
Mark PuderDepartment of Surgery and The Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Carlo BrugnaraDepartments of Pathology and Laboratory Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA carlo.brugnara@childrens.harvard.edu.
Lucia De FranceschiDepartment of Medicine, University of Verona-AOUI Verona, Policlinico GB Rossi, Verona, Italy.
University of Verona · ITUniversity of Turin · ITBoston Children's Hospital · USFederico II University Hospital · ITHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The anemia of sickle cell disease is associated with a severe inflammatory vasculopathy and endothelial dysfunction, which leads to painful and life-threatening clinical complications. Growing evidence supports the anti-inflammatory properties of ω-3 fatty acids in clinical models of endothelial dysfunction. Promising but limited studies show potential therapeutic effects of ω-3 fatty acid supplementation in sickle cell disease. Here, we treated humanized healthy and sickle cell mice for 6 weeks with ω-3 fatty acid diet (fish-oil diet). We found that a ω-3 fatty acid diet: (i) normalizes red cell membrane ω-6/ω-3 ratio; (ii) reduces neutrophil count; (iii) decreases endothelial activation by targeting endothelin-1 and (iv) improves left ventricular outflow tract dimensions. In a hypoxia-reoxygenation model of acute vaso-occlusive crisis, a ω-3 fatty acid diet reduced systemic and local inflammation and protected against sickle cell-related end-organ injury. Using isolated aortas from sickle cell mice exposed to hypoxia-reoxygenation, we demonstrated a direct impact of a ω-3 fatty acid diet on vascular activation, inflammation, and anti-oxidant systems. Our data provide the rationale for ω-3 dietary supplementation as a therapeutic intervention to reduce vascular dysfunction in sickle cell disease.

Indexed as

Dietary SupplementsAnemia, Sickle CellAnimalsAnti-Inflammatory AgentsBlood VesselsDisease Models, AnimalEndothelin-1Endothelium, VascularErythrocyte MembraneFatty Acids, Omega-3HumansHypoxiaMiceMice, TransgenicNeutrophilsOxygenAnti-Inflammatory AgentsEndothelin-1Fatty Acids, Omega-3Oxygen

Identifiers

PMID25934765
PMCPMC4486221
OpenAlexW2149270461

What OpenQuestion holds

Textmetadata
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.