Evidence map›Paper›PMID 26985016›Full record

ReviewTherapeutic advances in cardiovascular disease2016

Understanding mechanisms of hypertension in systemic lupus erythematosus.

Erin B Taylor, Michael J Ryan

Open access · bronzeAbstract readReview
In one paragraph

Review in Therapeutic advances in cardiovascular disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Guideline
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  10. Review
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  13. Article
  14. Lymphatics in Cardiovascular Physiology.Cold Spring Harbor perspectives in medicine · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Contribution of Th17 cells to tissue injury in hypertension.Current opinion in nephrology and hypertension · 2021
    Review
  20. Article
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

2 authors at 1 institution in 1 country.

Erin B TaylorDepartment of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA.
Michael J RyanDepartment of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA mjryan@umc.edu.
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI RECKELHOFF, JANE F · 1993 to 2018
$39.4M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
Renal mechanisms of hypertension in autoimmune disease I01BX002604 · VA · VETERANS HEALTH ADMINISTRATION · PI MICHAEL RYAN · 2015 to 2026
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BLRD VA I01 BX002604NHLBI NIH HHS P01 HL051971NHLBI NIH HHS T32 HL105324NIGMS NIH HHS P20 GM104357
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that predominately affects women of reproductive age. Hypertension is an important cardiovascular risk factor that is prevalent in this patient population. Despite the high incidence of hypertension in women with SLE, the pathophysiological mechanisms underlying the development of hypertension remain poorly understood. This review will focus on disease-related factors, including inflammation, autoantibodies, and sex hormones that may contribute to hypertension in patients with SLE. In addition, we will highlight studies performed by our laboratory using the female NZBWF1 (F1 hybrid of New Zealand Black and New Zealand White strains) mouse model, a spontaneous model of SLE that mimics human disease and develops hypertension and renal injury. Specifically, using female NZBWF1 mice, we have demonstrated that multiple factors contribute to the pathogenesis of hypertension, including the inflammatory cytokine, tumor necrosis factor (TNF)-α, oxidative stress, as well as B-cell hyperactivity and autoantibody production.

Indexed as

autoantibodiescardiovascular diseaseestrogenshypertensioninflammationsystemic lupus erythematosus

Identifiers

PMID26985016
PMCPMC5065379
OpenAlexW2301784842

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.