Evidence map›Paper›PMID 37897505›Full record

ArticleCardiovascular research2023

Deletion of adipocyte NOS3 potentiates high-fat diet-induced hypertension and vascular remodelling via chemerin.

Andy W C Man, Yawen Zhou, Gisela Reifenberg, Alica Camp, Thomas Münzel, Andreas Daiber, Ning Xia, Huige Li

Open access · hybridAbstract read
In one paragraph

Article in Cardiovascular research, 2023. 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
4.6field-weighted citation impact, top 4% 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, 21 citations in OpenAlex.

  1. Review
  2. Article
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  6. Article
  7. Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
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  16. Immune and Metabolic Mechanisms of Endothelial Dysfunction.International journal of molecular sciences · 2024
    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

8 authors at 1 institution in 1 country.

Andy W C ManDepartment of Pharmacology, Johannes Gutenberg University Medical Center, Langenbeckstr. 1, 55131 Mainz, Germany.ORCID 0000-0002-4113-6479
Yawen ZhouDepartment of Pharmacology, Johannes Gutenberg University Medical Center, Langenbeckstr. 1, 55131 Mainz, Germany.
Gisela ReifenbergDepartment of Pharmacology, Johannes Gutenberg University Medical Center, Langenbeckstr. 1, 55131 Mainz, Germany.
Alica CampDepartment of Pharmacology, Johannes Gutenberg University Medical Center, Langenbeckstr. 1, 55131 Mainz, Germany.
Thomas MünzelDepartment of Cardiology, Cardiology I, Johannes Gutenberg University Medical Center, Mainz, Germany.
Andreas DaiberDepartment of Cardiology, Cardiology I, Johannes Gutenberg University Medical Center, Mainz, Germany.ORCID 0000-0002-2769-0094
Ning XiaDepartment of Pharmacology, Johannes Gutenberg University Medical Center, Langenbeckstr. 1, 55131 Mainz, Germany.
Huige LiDepartment of Pharmacology, Johannes Gutenberg University Medical Center, Langenbeckstr. 1, 55131 Mainz, Germany.
Johannes Gutenberg University Mainz · DE

Funding

a TransMed Fellowship of Johannes Gutenberg University Medical CenterDeutsche Forschungsgemeinschaft LI-1042/5-1 (H.L.) and XI 139/2-1 (N.X.)DZHKGerman Centre for Cardiovascular Research
6 · The paper itself

Abstract

aimsObesity is an epidemic that is a critical contributor to hypertension and other cardiovascular diseases. Current paradigms suggest that endothelial nitric oxide synthase (eNOS/NOS3) in the vessel wall is the primary regulator of vascular function and blood pressure. However, recent studies have revealed the presence of eNOS/NOS3 in the adipocytes of white adipose tissues and perivascular adipose tissues (PVATs). The current understanding of the role of adipocyte NOS3 is based mainly on studies using global knockout models. The present study aimed to elucidate the functional significance of adipocyte NOS3 for vascular function and blood pressure control. METHODS AND

resultsWe generated an adipocyte-specific NOS3 knockout mouse line using adiponectin promoter-specific Cre-induced gene inactivation. Control and adipocyte-specific NOS3 knockout (A-NOS3 KO) mice were fed a high-fat diet (HFD). Despite less weight gain, A-NOS3 KO mice exhibited a significant increase in blood pressure after HFD feeding, associated with exacerbated vascular dysfunction and remodelling. A-NOS3 KO mice also showed increased expression of signature markers of inflammation and hypoxia in the PVATs. Among the differentially expressed adipokines, we have observed an upregulation of a novel adipokine, chemerin, in A-NOS3 KO mice. Chemerin was recently reported to link obesity and vascular dysfunction. Treatment with chemerin neutralizing antibody normalized the expression of remodelling markers in the aorta segments cultured in serum from HFD-fed A-NOS3 KO mice ex vivo.

conclusionThese data suggest that NOS3 in adipocytes is vital in maintaining vascular homeostasis; dysfunction of adipocyte NOS3 contributes to obesity-induced vascular remodelling and hypertension.

Indexed as

Diet, High-FatHypertensionNitric Oxide Synthase Type IIIAdipocytesAdipokinesAnimalsChemokinesIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutObesityVascular RemodelingAdipokineschemerin protein, mouseChemokinesIntercellular Signaling Peptides and ProteinsNitric Oxide Synthase Type IIIAdipokineAdipose tissueCross-talkEndothelial functionOxidative stress

Identifiers

PMID37897505
PMCPMC10757584
OpenAlexW4388007081

What Socratic 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 Socratic graph.