Evidence map›Paper›PMID 25712723›Full record

ArticleHypertension (Dallas, Tex. : 1979)2015

Exposure to experimental preeclampsia in mice enhances the vascular response to future injury.

Dafina Pruthi, Eliyahu V Khankin, Robert M Blanton, Mark Aronovitz, Suzanne D Burke, Amy McCurley, S Ananth Karumanchi, Iris Z Jaffe

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

47 citing papers in PubMed, 93 citations in OpenAlex.

  1. Trial
  2. The pathophysiology of pre-eclampsia.Nature reviews. Nephrology · 2026
    Review
  3. Transforming Preeclampsia Care: Molecular Diagnostics and Therapeutic Innovations.Journal of the American Society of Nephrology : JASN · 2026
    Review
  4. Article
  5. Cardiac Implications of Preeclampsia: A Review.Journal of personalized medicine · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Metabolic theory of preeclampsia: implications for maternal cardiovascular health.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  11. Early- to mid-gestational testosterone excess leads to adverse cardiac outcomes in postpartum sheep.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  12. Postpartum and interpregnancy care of women with a history of hypertensive disorders of pregnancy.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Placental syndromes and maternal cardiovascular health.Clinical science (London, England : 1979) · 2023
    Review
  18. Review
  19. 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

8 authors at 2 institutions in 1 country.

Dafina PruthiFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.).
Eliyahu V KhankinFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.).
Robert M BlantonFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.).
Mark AronovitzFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.).
Suzanne D BurkeFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.).
Amy McCurleyFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.).
S Ananth KarumanchiFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.). ijaffe@tuftsmedicalcenter.org sananth@bidmc.harvard.edu.
Iris Z JaffeFrom the Molecular Cardiology Research Institute (D.P., R.M.B., M.A., A.M., I.Z.J.) and Division of Cardiology, Department of Medicine (R.M.B., I.Z.J.), Tufts Medical Center, Boston, MA; Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (E.V.K., S.D.B., S.A.K.); and Howard Hughes Medical Institute, Chevy Chase, MD (S.D.B., S.A.K.). ijaffe@tuftsmedicalcenter.org sananth@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

The Role of Vascular MR-Regulated Genes in Vascular Function and DiseaseR01HL095590 · NHLBI · TUFTS MEDICAL CENTER · PI Iris Z Jaffe · 2009 to 2026
$7.7M
Smooth Muscle Mineralocorticoid Receptors in Vascular Aging and HypertensionR01HL119290 · NHLBI · TUFTS MEDICAL CENTER · PI Iris Z Jaffe · 2014 to 2026
$7.0M
Training Program in Cardiovascular ResearchT32HL069770 · NHLBI · TUFTS MEDICAL CENTER · PI KARAS, RICHARD H · 2003 to 2013
$4.7M
Preeclampsia and renal complications: late effects on kidney and vasculatureK08DK101560 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KHANKIN, ELIYAHU · 2014 to 2017
$616k
Howard Hughes Medical InstituteNHLBI NIH HHS HL095590NHLBI NIH HHS R01 HL095590NHLBI NIH HHS R01 HL119290NHLBI NIH HHS T32 HL069770NIDDK NIH HHS 1K08DK101560-01NIDDK NIH HHS K08 DK101560
6 · The paper itself

Abstract

Cardiovascular disease (CVD) remains the leading killer of women in developed nations. One sex-specific risk factor is preeclampsia, a syndrome of hypertension and proteinuria that complicates 5% of pregnancies. Although preeclampsia resolves after delivery, exposed women are at increased long-term risk of premature CVD and mortality. Pre-existing CVD risk factors are associated with increased risk of developing preeclampsia but whether preeclampsia merely uncovers risk or contributes directly to future CVD remains a critical unanswered question. A mouse preeclampsia model was used to test the hypothesis that preeclampsia causes an enhanced vascular response to future vessel injury. A preeclampsia-like state was induced in pregnant CD1 mice by overexpressing soluble fms-like tyrosine kinase-1, a circulating antiangiogenic protein that induces hypertension and glomerular disease resembling human preeclampsia. Two months postpartum, soluble fms-like tyrosine kinase-1 levels and blood pressure normalized and cardiac size and function by echocardiography and renal histology were indistinguishable in preeclampsia-exposed compared with control mice. Mice were then challenged with unilateral carotid injury. Preeclampsia-exposed mice had significantly enhanced vascular remodeling with increased vascular smooth muscle cell proliferation (180% increase; P<0.01) and vessel fibrosis (216% increase; P<0.001) compared with control pregnancy. In the contralateral uninjured vessel, there was no difference in remodeling after exposure to preeclampsia. These data support a new model in which vessels exposed to preeclampsia retain a persistently enhanced vascular response to injury despite resolution of preeclampsia after delivery. This new paradigm may contribute to the substantially increased risk of CVD in woman exposed to preeclampsia.

Indexed as

Pregnancy, AnimalRecovery of FunctionVascular RemodelingAnimalsBlood PressureCarotid ArteriesCarotid Artery DiseasesDisease Models, AnimalFemaleMicePostpartum PeriodPre-EclampsiaPregnancyUltrasonographycardiovascular diseaseshypertensionpreeclampsiavascular remodelingVEGF receptor flt-1 protein

Identifiers

PMID25712723
PMCPMC4359068
OpenAlexW1969689988

What OpenQuestion holds

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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.