Evidence map›Paper›PMID 33576385›Full record

ArticleCardiovascular research2022

Deficiency of inactive rhomboid protein 2 (iRhom2) attenuates diet-induced hyperlipidaemia and early atherogenesis.

Carmen Hannemann, Johannes H Schecker, Alica Brettschneider, Jana Grune, Nicole Rösener, Andrea Weller, Verena Stangl, Edward A Fisher, Karl Stangl, Antje Ludwig and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 41% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

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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 at 2 institutions in 2 countries.

Carmen HannemannCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.ORCID 0000-0002-2573-0152
Johannes H ScheckerCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.ORCID 0000-0001-9392-6969
Alica BrettschneiderCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.
Jana GruneDZHK (German Centre for Cardiovascular Research), partner site Berlin, Charitéplatz 1, 10117 Berlin, Germany.
Nicole RösenerCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.
Andrea WellerCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.ORCID 0000-0001-7126-0916
Verena StanglCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.
Edward A FisherDivision of Cardiology, Department of Medicine, New York University School of Medicine, Hannemann435 East 30th St., 10016 New York, NY, USA.ORCID 0000-0001-9802-143X
Karl StanglCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.
Antje LudwigCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.
Bernd HewingCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charitéplatz 1, 10117 Berlin, Germany.ORCID 0000-0003-3734-2533
Humboldt-Universität zu Berlin · DENew York University · US

Funding

Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
NHLBI NIH HHS R01 HL084312
6 · The paper itself

Abstract

aimsAtherosclerosis is a chronic inflammatory disease of the arterial vessel wall and anti-inflammatory treatment strategies are currently pursued to lower cardiovascular disease burden. Modulation of recently discovered inactive rhomboid protein 2 (iRhom2) attenuates shedding of tumour necrosis factor-alpha (TNF-α) selectively from immune cells. The present study aims at investigating the impact of iRhom2 deficiency on the development of atherosclerosis. METHODS AND

resultsLow-density lipoprotein receptor (LDLR)-deficient mice with additional deficiency of iRhom2 (LDLR-/-iRhom2-/-) and control (LDLR-/-) mice were fed a Western-type diet (WD) for 8 or 20 weeks to induce early or advanced atherosclerosis. Deficiency of iRhom2 resulted in a significant decrease in the size of early atherosclerotic plaques as determined in aortic root cross-sections. LDLR-/-iRhom2-/- mice exhibited significantly lower serum levels of TNF-α and lower circulating and hepatic levels of cholesterol and triglycerides compared to LDLR-/- mice at 8 weeks of WD. Analyses of hepatic bile acid concentration and gene expression at 8 weeks of WD revealed that iRhom2 deficiency prevented WD-induced repression of hepatic bile acid synthesis in LDLR-/- mice. In contrast, at 20 weeks of WD, plaque size, plaque composition, and serum levels of TNF-α or cholesterol were not different between genotypes.

conclusionModulation of inflammation by iRhom2 deficiency attenuated diet-induced hyperlipidaemia and early atherogenesis in LDLR-/- mice. iRhom2 deficiency did not affect diet-induced plaque burden and composition in advanced atherosclerosis in LDLR-/- mice.

Indexed as

AnimalsAortaAortic DiseasesAtherosclerosisBile Acids and SaltsCarrier ProteinsCytokinesDiet, High-FatDisease Models, AnimalHyperlipidemiasInflammation MediatorsLipidsLiverMaleMiceMice, Inbred C57BLBile Acids and SaltsCarrier ProteinsCytokinesInflammation MediatorsiRhom2 protein, mouseLipidsReceptors, LDLAtherosclerosisInflammationiRhom2/Rhbdf2TNF-alpha

Identifiers

PMID33576385
PMCPMC8932158
OpenAlexW3126545835

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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.