Evidence map›Paper›PMID 38199832›Full record

ArticleAmerican heart journal2024

Burden of cardiometabolic risk factors and vascular health.

Carine E Hamo, Florencia Schlamp, Kamelia Drenkova, Manila Jindal, Maja Fadzan, Adedoyin Akinlonu, Ira Goldberg, Michael S Garshick, Jeffrey S Berger

Open access · greenAbstract read
In one paragraph

Article in American heart journal, 2024. 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
2.0field-weighted citation impact, top 14% 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, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. CEACAM1 in vascular homeostasis and inflammation.European journal of clinical investigation · 2024
    Review
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

9 authors at 2 institutions in 1 country.

Carine E HamoDepartment of Medicine, Center for the Prevention of Cardiovascular Disease, New York University School of Medicine, New York City, NY; Leon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY. Electronic address: carine.hamo@nyulangone.org.
Florencia SchlampLeon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
Kamelia DrenkovaLeon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
Manila JindalLeon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
Maja FadzanLeon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
Adedoyin AkinlonuLeon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
Ira GoldbergDepartment of Medicine, Center for the Prevention of Cardiovascular Disease, New York University School of Medicine, New York City, NY; Leon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
Michael S GarshickDepartment of Medicine, Center for the Prevention of Cardiovascular Disease, New York University School of Medicine, New York City, NY; Leon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
Jeffrey S BergerDepartment of Medicine, Center for the Prevention of Cardiovascular Disease, New York University School of Medicine, New York City, NY; Leon H. Charney Division of Cardiology, Department of Medicine, Cardiovascular Research Center, New York University School of Medicine, New York City, NY.
New York University · USCity University of New York · US

Funding

Training Program in Cardiovascular SciencesT32HL098129 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Glenn I Fishman, Ira J Goldberg · 2009 to 2026
$5.9M
Mechanisms of Platelet Activity in Vascular DiseaseR35HL144993 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BERGER, JEFFREY S · 2019 to 2025
$5.5M
Endovascular Health and Platelet Activity in PsoriasisK23HL152013 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI GARSHICK, MICHAEL SETH · 2021 to 2025
$865k
NHLBI NIH HHS K23 HL152013NHLBI NIH HHS L30 HL143703NHLBI NIH HHS R35 HL144993NHLBI NIH HHS T32 HL098129
6 · The paper itself

Abstract

backgroundCardiometabolic risk factors diabetes, obesity, and hypertension are highly prevalent and contribute to increased cardiovascular disease (CVD). Endothelial dysfunction precedes CVD development. The current study aimed to investigate the EC transcriptome among individuals with varying degree of cardiometabolic risk.

methodsAdult participants without CVD and various degrees of cardiometabolic risk factor burden (hypertension, diabetes, obesity) were included. Participants underwent brachial vein EC harvesting followed by RNA sequencing. To evaluate the association between cardiometabolic comorbidity burden and outcome transcripts we performed linear regression with multivariable models, adjusting for age, sex, and race/ethnicity.

resultsA total of 18 individuals were included in the present analysis (mean age 47 ± 14, 44% female, and 61% White adults). Endothelial cell RNA sequencing revealed 588 differentially expressed transcripts (p-adj <0.05) with excellent discrimination in unsupervised hierarchical clustering analysis. Gene ontology enrichment analysis revealed upregulated pathways associated with T-cell activation (NES = 2.22, p<0.001), leukocyte differentiation (NES= 2.16, p<0.001), leukocyte migration (NES= 2.12, p<0.001), regulation of cell-cell adhesion (NES= 1.91, p=0.006). Downregulated pathways of interest included endothelial cell proliferation (NES= -1.68, p=0.03) and response to interleukin-1 (NES= -1.61, p=0.04). Upregulated genes included VCAM1, CEACAM1, ADAM 17, and CD99L2, all with a log-2-fold change >3 and p-adj <0.05. These genes demonstrated a graded increase in mean normalized counts with increasing number of risk factors.

conclusionsWe demonstrate a proinflammatory and pro-adhesive EC transcriptome associated with increased cardiometabolic risk factor burden offering insight into a potential mechanism linking these risk factors with the development of CVD.

Indexed as

Cardiovascular DiseasesDiabetes MellitusHypertensionAdultCardiometabolic Risk FactorsFemaleHumansMaleMiddle AgedObesityRisk Factors

Identifiers

PMID38199832
PMCPMC10922119
OpenAlexW4390599398

What OpenQuestion holds

Textmetadata
LicenceTDM
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.