Evidence map›Paper›PMID 29485737›Full record

ReviewClinical cardiology2018

Hypertension in pregnancy: Taking cues from pathophysiology for clinical practice.

Ruxandra I Sava, Keith L March, Carl J Pepine

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 69 citations in OpenAlex.

  1. Observational
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Hypertensive disorders of pregnancy: definition, management, and out-of-office blood pressure measurement.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Placental hypoxia-induced alterations in vascular function, morphology, and endothelial barrier integrity.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Article
  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

3 authors at 2 institutions in 2 countries.

Ruxandra I SavaCenter for Regenerative Medicine, University of Florida, Gainesville, Florida.
Keith L MarchCenter for Regenerative Medicine, University of Florida, Gainesville, Florida.
Carl J PepineCenter for Regenerative Medicine, University of Florida, Gainesville, Florida.ORCID http://orcid.org/0000-0002-6011-681X
University of Florida · USCarol Davila University of Medicine and Pharmacy · RO

Funding

Using social networks to map and evaluate team science across CTSA hubsUL1TR001427 · NCATS · UNIVERSITY OF FLORIDA · PI MITCHELL, DUANE A. · 2015 to 2024
$37.2M
Data Coordinating Center For The Cardiovascular Cell Therapy Research NetworkUM1HL087318 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DAVIS, BARRY R · 2012 to 2018
$29.8M
UFRCC for Cardiovascular Cell Therapy Research NetworkUM1HL087366 · NHLBI · UNIVERSITY OF FLORIDA · PI PEPINE, CARL J · 2012 to 2018
$4.7M
Brain-Gut Microbiome-Immune Axis in HypertensionR01HL132448 · NHLBI · UNIVERSITY OF FLORIDA · PI Carl J Pepine, Steven Michael Smith · 2016 to 2026
$4.5M
NCATS NIH HHS UL1 TR001427NHLBI NIH HHS R01 HL132448NHLBI NIH HHS UM1 HL087318NHLBI NIH HHS UM1 HL087366
6 · The paper itself

Abstract

Pregnancy-related hypertension (PHTN) syndromes are a frequent and potentially deadly complication of pregnancy, while also negatively impacting the lifelong health of the mother and child. PHTN appears in women likely to develop hypertension later in life, with the stress of pregnancy unmasking a subclinical hypertensive phenotype. However, distinguishing between PHTN and chronic hypertension is essential for optimal management. Preeclampsia (PE) is linked to potentially severe outcomes and lacks effective treatments due to poorly understood mechanisms. Inadequate remodeling of spiral uterine arteries (SUAs), the cornerstone of PE pathophysiology, leads to hypoperfusion of the developing placenta. In normal pregnancies, extravillous trophoblast (EVT) cells assume an invasive phenotype and invade SUAs, transforming them into large conduits. Decidual natural killer cells play an essential role, mediating materno-fetal immune tolerance, inducing early SUA remodeling and regulating EVT invasiveness. Notch signaling is important in EVT phenotypic switch and is dysregulated in PE. The hypoxic placenta releases antiangiogenic and proinflammatory factors that converge upon maternal endothelium, inducing endothelial dysfunction, hypertension, and organ damage. Hypoxia-inducible factor 1-α is upstream of such molecules, whereas endothelin-1 is a major effector. We also describe important genetic links and evidence of incomplete materno-fetal immune tolerance, with PE patients presenting with autoantibodies, lower T

Indexed as

Disease ManagementPre-EclampsiaRisk AssessmentBlood PressureFemaleGlobal HealthHumansIncidencePregnancySurvival RateDecidual Natural Killer CellsExtravillous Trophoblast CellsHypoxiaIncomplete Materno-Fetal Immune TolerancePreeclampsia

Identifiers

PMID29485737
PMCPMC6490052
OpenAlexW2790209252

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.