ArticlePregnancy hypertension2019
Renal natural killer cell activation and mitochondrial oxidative stress; new mechanisms in AT1-AA mediated hypertensive pregnancy.
Article in Pregnancy hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Sex differences in the developmental programming of cardiovascular and renal risk across the lifespan.American journal of physiology. Renal physiology · 2026Review
- The Pathogenesis of Preeclampsia: Hypoxia and the Unfolded Protein Response.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- AT1-AA induced hypertension during pregnancy contributes to developmental programming of hypertension in female offspring.Journal of reproductive immunology · 2025Article
- Uncovering immune pathways for therapeutic targeting of hypertension.Expert opinion on therapeutic targets · 2025Review
- Role of agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA) in pathogenesis of preeclampsia.Global medical genetics · 2025Review
- Intrauterine growth-restricted pregnant rats, from placental ischemic dams, display preeclamptic-like symptoms: A new rat model of preeclampsia.Physiological reports · 2024Article
- Transcutaneous Auricular Vagus Nerve Stimulation Ameliorates Preeclampsia-Induced Apoptosis of Placental Trophoblastic Cells Via Inhibiting the Mitochondrial Unfolded Protein Response.Neuroscience bulletin · 2024Article
- Metabolic theory of preeclampsia: implications for maternal cardiovascular health.American journal of physiology. Heart and circulatory physiology · 2024Review
- The role of T cell stimulated agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) in mediating multiorgan dysfunction in IL-17 induced hypertension during pregnancy.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Article
- Placental and Renal Pathways Underlying Pre-Eclampsia.International journal of molecular sciences · 2024Review
- 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
- Differential expression of the angiotensin receptors (AT1, AT2, and AT4) in the placental bed of HIV-infected preeclamptic women of African ancestry.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- RUPP Th17s cause hypertension and mitochondrial dysfunction in the kidney and placenta during pregnancy.Pregnancy hypertension · 2023Article
- Inhibition of angiotensin II type 1 receptor agonistic autoantibodies by direct binding does not impact reduced uterine perfusion pressure offspring birthweight and blood pressure at adulthood.American journal of obstetrics & gynecology MFM · 2023Article
- 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
- AT1-AA Infusion during Pregnancy Impairs CBF Autoregulation Postpartum.International journal of cerebrovascular disease and stroke · 2023Article
- Review
- Animal models of preeclampsia: investigating pathophysiology and therapeutic targets.American journal of obstetrics and gynecology · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Women with preeclampsia (PE) have increased mean arterial pressure (MAP), natural killer (NK) cells, reactive oxygen species (ROS), and agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA). AT1-AA's administered to pregnant rodents produces a well-accepted model of PE. However, the role of NK cells and mitochondrial reactive oxygen species (mtROS) in AT1-AA mediated hypertension during pregnancy is unknown. We hypothesize that AT1-AA induced model of PE will exhibit elevated MAP, NK cells, and mtROS; while inhibition of the AT1-AA binding to the AT1R would be preventative. Pregnant rats were divided into 4 groups: normal pregnant (NP) (n = 5), NP + AT1-AA inhibitory peptide (NP +'n7AAc') (n = 3), NP + AT1-AA infused (NP + AT1-AA) (n = 10), and NP + AT1-AA +'n7AAc' (n = 8). Day 13, rats were surgically implanted with mini-pumps infusing either AT1-AA or AT1-AA +'n7AAc'. Day 19, tissue and blood was collected. MAP was elevated in AT1-AA vs. NP (119 ± 1 vs. 102 ± 2 mmHg, p < 0.05) and this was prevented by 'n7AAc' (108 ± 3). There was a 6 fold increase in renal activated NK cells in AT1-AA vs NP (1.2 ± 0.4 vs. 0.2 ± 0.1% Gated, p = 0.05) which returned to NP levels in AT1-AA +'n7AAc' (0.1 ± 0.1% Gated). Renal mtROS (317 ± 49 vs. 101 ± 13% Fold, p < 0.05) was elevated with AT1-AA vs NP and was decreased in AT1-AA +'n7AAc' (128 ± 16, p < 0.05). In conclusion, AT1-AA's increased MAP, NK cells, and mtROS which were attenuated by AT1-AA inhibition, thus highlighting new mechanisms of AT1-AA and the importance of drug therapy targeted to AT1-AAs in hypertensive pregnancies.
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