ArticleAmerican journal of physiology. Renal physiology2021
CD4+ T cells cause renal and placental mitochondrial oxidative stress as mechanisms of hypertension in response to placental ischemia.
Article in American journal of physiology. Renal physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.
- Reduced uterine perfusion pressure as a model for preeclampsia and fetal growth restriction in murine: a systematic review and meta-analysis.American journal of physiology. Heart and circulatory physiology · 2024Pooled it
- Analysis of the evolution of placental oxidative stress research from a bibliometric perspective.Frontiers in pharmacology · 2024Pooled it
- Identification of diagnostic biomarkers and mitochondrial metabolic characteristics in sepsis-associated acute kidney injury.European journal of medical research · 2025Article
- Comprehensive identification of immune-related biomarkers and therapeutic targets in preeclampsia: integrative bioinformatics and experimental validation.BMC pregnancy and childbirth · 2025Article
- Oxidative Stress and Inflammation in Uterine-Vascular Adaptation During Pregnancy.Antioxidants (Basel, Switzerland) · 2025Review
- The Role of Mitochondrial Dysfunction and Oxidative Stress in Women's Reproductive Disorders: Implications for Polycystic Ovary Syndrome and Preeclampsia.International journal of molecular sciences · 2025Review
- Article
- Ferroptosis-related genes in preeclampsia: integrative bioinformatics analysis, experimental validation and drug prediction.BMC pregnancy and childbirth · 2025Article
- Identification and validation of key biomarkers associated with immune and oxidative stress for preeclampsia by WGCNA and machine learning.Frontiers in genetics · 2025Article
- Intact NOX2 in T Cells Mediates Pregnancy-Induced Renal Damage in Dahl SS Rats.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Abatacept Decreases Renal T-cell Infiltration and Renal Inflammation and Ameliorates Progressive Renal Injury in Obese Dahl Salt-sensitive Rats Before Puberty.Journal of cardiovascular pharmacology · 2024Article
- AT1-AA Is Produced in Offspring in Response to Placental Ischemia and Is Lowered by B-Cell Depletion Without Compromising Overall Offspring Health.Journal of the American Heart Association · 2024Article
- Inhibiting B cell activating factor attenuates preeclamptic symptoms in placental ischemic rats.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- The role of immune cells and mediators in preeclampsia.Nature reviews. Nephrology · 2023Review
- B2 cells contribute to hypertension and natural killer cell activation possibly via AT1-AA in response to placental ischemia.American journal of physiology. Renal physiology · 2023Article
- Article
- Setting a stage: Inflammation during preeclampsia and postpartum.Frontiers in physiology · 2023Review
- Review
- Abnormal Expression of the LAG-3/FGL-1 Signaling Pathway in Patients with Early-Onset Preeclampsia.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Is Mitochondrial Oxidative Stress a Viable Therapeutic Target in Preeclampsia?Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The reduced uterine perfusion pressure (RUPP) rat model and normal pregnant (NP) rat recipients of RUPP CD4+ T cells recapitulate many characteristics of preeclampsia such as hypertension and oxidative stress. We have shown an important hypertensive role for natural killer (NK) cells to cause mitochondrial dysfunction in RUPP rats; however, the role for RUPP CD4+ T cells to stimulate NK cells is unknown. Therefore, we hypothesized that RUPP-induced CD4+ T cells activate NK cells to cause mitochondrial dysfunction/reactive oxygen species (ROS) as mechanisms of hypertension during pregnancy. We tested our hypothesis by adoptive transfer of RUPP CD4+ T cells into NP rats or by inhibiting the activation of RUPP CD4+ T cells with Orencia (abatacept) and examining hypertension, NK cells, and mitochondrial function. RUPP was performed on gestation day (GD) 14, and splenic CD4+ T cells were isolated on GD 19 and injected into NP rats on GD 13. In a separate group of rats, Orencia was infused and the RUPP procedure was performed. Mean arterial pressure and placental and renal mitochondrial ROS increased in RUPP (
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.