Evidence map›Paper›PMID 33417666›Full record

ReviewAmerican journal of hypertension2021

The Role of Mitochondrial Dysfunction in Preeclampsia: Causative Factor or Collateral Damage?

Alex N Smith, Xi Wang, Daniel G Thomas, Robert E Tatum, George W Booz, Mark W Cunningham

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of hypertension, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Knowledge-Driven Mechanistic Enrichment of the Preeclampsia Ignorome.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2023
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Subtype specific immune-metabolic reprogramming in preeclampsia revealed by multiomics and serum biomarkers.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  6. PeerJ · 2026
    Article
  7. Review
  8. Placental mitochondria in high-altitude pregnancy: metabolic adaptations and a toolkit for respiratory assessment.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  9. YME1L1 Dysfunction Associated With 3-Methylglutaconic Aciduria.Journal of inherited metabolic disease · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Metabolic theory of preeclampsia: implications for maternal cardiovascular health.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  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

6 authors at 1 institution in 1 country.

Alex N SmithDepartment of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.ORCID 0000-0001-5990-6964
Xi WangDepartment of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Daniel G ThomasDepartment of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Robert E TatumDepartment of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
George W BoozDepartment of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Mark W CunninghamDepartment of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.ORCID 0000-0001-5990-6964
University of Mississippi Medical Center · US

Funding

American Heart Association-American Stroke Association 18CDA34110264
6 · The paper itself

Abstract

Preeclampsia, new onset hypertension in pregnancy, affects ~5%-10% of the world's population. Preeclampsia is the leading cause of morbidity and mortality for both the mother and fetus. As of today, there is no cure for this disease except for delivery of the fetal-placental unit. The exact causation and onset of the disease are unknown. However, recent studies have shown a strong correlation between mitochondrial dysfunction and preeclampsia. Circulating mitochondrial DNA, elevated reactive oxygen species, angiotensin II type 1 receptor agonistic autoantibodies (AT1-AA), activated natural killer cells, and upregulated inflammatory responses all contribute to mitochondrial dysfunction and the pathophysiology of preeclampsia. This review summarizes the current literature of both experimental and clinical observations that support the hypothesis that mitochondrial dysfunction contributes to the pathophysiology of preeclampsia and may be a precursor to the disease onset. This review will also address the use of therapies to improve mitochondrial dysfunction in preeclampsia.

Indexed as

MitochondriaPre-EclampsiaFemaleHumansPregnancyblood pressureendothelial dysfunctionhypertensioninflammationinnate immunitymitochondrial dysfunctionnatural killer cellsoxidative stresspreeclampsia

Identifiers

PMID33417666
PMCPMC12379711
OpenAlexW3120921153

What Socratic 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 Socratic graph.