Evidence map›Paper›PMID 31327268›Full record

ArticleHypertension (Dallas, Tex. : 1979)2019

Camk2n1 Is a Negative Regulator of Blood Pressure, Left Ventricular Mass, Insulin Sensitivity, and Promotes Adiposity.

Neza Alfazema, Marjorie Barrier, Sophie Marion de Procé, Robert I Menzies, Roderick Carter, Kevin Stewart, Ana Garcia Diaz, Ben Moyon, Zoe Webster, Christopher O C Bellamy and 5 more

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

Article in Hypertension (Dallas, Tex. : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Tale of two kinases: Protein kinase A and CaWorld journal of diabetes · 2021
    Review
  4. Article
  5. Review
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 1 country.

Neza AlfazemaFrom the MRC Institute of Genetics and Molecular Medicine, Edinburgh, United Kingdom (N.A., M.B., S.M.d.P., T.J.A., P.M.C.).
Marjorie BarrierFrom the MRC Institute of Genetics and Molecular Medicine, Edinburgh, United Kingdom (N.A., M.B., S.M.d.P., T.J.A., P.M.C.).
Sophie Marion de ProcéFrom the MRC Institute of Genetics and Molecular Medicine, Edinburgh, United Kingdom (N.A., M.B., S.M.d.P., T.J.A., P.M.C.).
Robert I MenziesCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, United Kingdom (R.I.M., R.C., K.S., R.H.S., N.M.M.).
Roderick CarterCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, United Kingdom (R.I.M., R.C., K.S., R.H.S., N.M.M.).
Kevin StewartCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, United Kingdom (R.I.M., R.C., K.S., R.H.S., N.M.M.).
Ana Garcia DiazMRC London Institute of Medical Sciences, Imperial College London, United Kingdom (A.G.D., B.M., Z.W.).
Ben MoyonMRC London Institute of Medical Sciences, Imperial College London, United Kingdom (A.G.D., B.M., Z.W.).
Zoe WebsterMRC London Institute of Medical Sciences, Imperial College London, United Kingdom (A.G.D., B.M., Z.W.).
Christopher O C BellamyDivision of Pathology, Centre for Comparative Pathology, Edinburgh CRUK Cancer Centre, United Kingdom (C.O.C.B., M.J.A.).
Mark J ArendsDivision of Pathology, Centre for Comparative Pathology, Edinburgh CRUK Cancer Centre, United Kingdom (C.O.C.B., M.J.A.).
Roland H StimsonCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, United Kingdom (R.I.M., R.C., K.S., R.H.S., N.M.M.).
Nicholas M MortonCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, United Kingdom (R.I.M., R.C., K.S., R.H.S., N.M.M.).
Timothy J AitmanFrom the MRC Institute of Genetics and Molecular Medicine, Edinburgh, United Kingdom (N.A., M.B., S.M.d.P., T.J.A., P.M.C.).
Philip M CoanFrom the MRC Institute of Genetics and Molecular Medicine, Edinburgh, United Kingdom (N.A., M.B., S.M.d.P., T.J.A., P.M.C.).
MRC Institute of Genetics and Molecular Medicine · GBThe Queen's Medical Research Institute · GBMRC London Institute of Medical Sciences · GBUniversity of Edinburgh · GB

Funding

Medical Research Council MR/K010271/1Medical Research Council MR/N005902/1
6 · The paper itself

Abstract

Metabolic syndrome is a cause of coronary artery disease and type 2 diabetes mellitus. Camk2n1 resides in genomic loci for blood pressure, left ventricle mass, and type 2 diabetes mellitus, and in the spontaneously hypertensive rat model of metabolic syndrome, Camk2n1 expression is cis-regulated in left ventricle and fat and positively correlates with adiposity. Therefore, we knocked out Camk2n1 in spontaneously hypertensive rat to investigate its role in metabolic syndrome. Compared with spontaneously hypertensive rat, Camk2n1

Indexed as

AdiposityAnimalsCalcium-Binding ProteinsCarrier ProteinsDiabetes Mellitus, Type 2Disease Models, AnimalGene Expression RegulationHumansHypertensionHypertrophy, Left VentricularMetabolic SyndromeRandom AllocationRatsRats, Inbred SHRRisk AssessmentSensitivity and SpecificityCalcium-Binding ProteinsCamk2n1 protein, ratCarrier Proteinsadiposityblood pressurehypertrophymetabolic syndromerats

Identifiers

PMID31327268
PMCPMC6686962
OpenAlexW2962951989

What OpenQuestion 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 OpenQuestion graph.