Evidence map›Paper›PMID 26569331›Full record

ReviewBiomolecules2015

Immune Mechanisms Linking Obesity and Preeclampsia.

Frank T Spradley, Ana C Palei, Joey P Granger

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
9.1field-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

42 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Gestational diabetes status modifies pre-pregnancy BMI associations with large for gestational age: A prospective cohort study in central China.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026
    Article
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Pathophysiology of Maternal Obesity and Hypertension in Pregnancy.Journal of cardiovascular development and disease · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. How can we reduce maternal mortality due to preeclampsia? The 4P rule.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2024
    Review
  13. Article
  14. Review
  15. Article
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  18. Review
  19. Article
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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 1 institution in 1 country.

Frank T SpradleyDepartment of Physiology and Biophysics, Cardiovascular-Renal Research Center, Women's Health Research Center, The University of Mississippi Medical Center, Jackson, MS 39216, USA. fspradley@umc.edu.
Ana C PaleiDepartment of Physiology and Biophysics, Cardiovascular-Renal Research Center, Women's Health Research Center, The University of Mississippi Medical Center, Jackson, MS 39216, USA. apalei@umc.edu.
Joey P GrangerDepartment of Physiology and Biophysics, Cardiovascular-Renal Research Center, Women's Health Research Center, The University of Mississippi Medical Center, Jackson, MS 39216, USA. jgranger@umc.edu.
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HALL, JOHN E · 1993 to 2018
$39.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
NHLBI NIH HHS 2P01-HL51971NHLBI NIH HHS 2T32HL105324-06NHLBI NIH HHS P01 HL051971NHLBI NIH HHS T32 HL105324
6 · The paper itself

Abstract

Preeclampsia (PE) is characterized by hypertension occurring after the twentieth week of pregnancy. It is a significant contributor to maternal and perinatal morbidity and mortality in developing countries and its pervasiveness is increasing within developed countries including the USA. However, the mechanisms mediating the pathogenesis of this maternal disorder and its rising prevalence are far from clear. A major theory with strong experimental evidence is that placental ischemia, resulting from inappropriate remodeling and widening of the maternal spiral arteries, stimulates the release of soluble factors from the ischemic placenta causing maternal endothelial dysfunction and hypertension. Aberrant maternal immune responses and inflammation have been implicated in each of these stages in the cascade leading to PE. Regarding the increased prevalence of this disease, it is becoming increasingly evident from epidemiological data that obesity, which is a state of chronic inflammation in itself, increases the risk for PE. Although the specific mechanisms whereby obesity increases the rate of PE are unclear, there are strong candidates including activated macrophages and natural killer cells within the uterus and placenta and activation in the periphery of T helper cells producing cytokines including TNF-α, IL-6 and IL-17 and the anti-angiogenic factor sFlt-1 and B cells producing the agonistic autoantibodies to the angiotensin type 1 receptor (AT1-aa). This review will focus on the immune mechanisms that have been implicated in the pathogenesis of hypertension in PE with an emphasis on the potential importance of inflammatory factors in the increased risk of developing PE in obese pregnancies.

Indexed as

AnimalsCytokinesEndothelin-1FemaleHumansObesityPre-EclampsiaPregnancyCytokinesEndothelin-1Adiposeantibodyendothelinhypertensionlymphocytepregnancy

Identifiers

PMID26569331
PMCPMC4693273
OpenAlexW2176104324

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.