Evidence map›Paper›PMID 27097659›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

Identifying immune mechanisms mediating the hypertension during preeclampsia.

Babbette LaMarca, Denise C Cornelius, Ashlyn C Harmon, Lorena M Amaral, Mark W Cunningham, Jessica L Faulkner, Kedra Wallace

Abstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
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

56 citing papers in PubMed.

  1. Review
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  12. Mononuclear Cells Negatively Regulate Endothelial CaReproductive sciences (Thousand Oaks, Calif.) · 2023
    Article
  13. Review
  14. Inhibiting B cell activating factor attenuates preeclamptic symptoms in placental ischemic rats.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023
    Article
  15. Article
  16. Review
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  18. Review
  19. Article
  20. Regulatory T Cell Apoptosis during Preeclampsia May Be Prevented by Gal-2.International journal of molecular sciences · 2022
    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

7 authors.

Babbette LaMarcaDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi bblamarca@umc.edu.
Denise C CorneliusDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Ashlyn C HarmonDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Lorena M AmaralDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Mark W CunninghamDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Jessica L FaulknerDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Kedra WallaceDepartment of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi.

Funding

Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
The Kidney, Hypertension, Pregnancy and InflammationR01HD067541 · NICHD · UNIVERSITY OF MISSISSIPPI MED CTR · PI LAMARCA, BABBETTE · 2011 to 2020
$3.1M
NHLBI NIH HHS T32 HL105324NICHD NIH HHS R01 HD067541
6 · The paper itself

Abstract

Preeclampsia (PE) is a pregnancy-associated disorder that affects 5-8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role.

Indexed as

AdultFemaleHumansHypertension, Pregnancy-InducedPre-EclampsiaPregnancyT-Lymphocytescytokineshypertensioninflammationpregnancy

Identifiers

PMID27097659
PMCPMC4967235

What OpenQuestion holds

Textmetadata
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.