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The role of inflammation in the pathology of preeclampsia

Clinical science (1979), 2016-03, Vol.130 (6), p.409

2016

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Pathophysiology and Current Clinical Management of Preeclampsia

Current hypertension reports, 2017-08, Vol.19 (8), p.61-61, Article 61

2017

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Inflammatory mediators: a causal link to hypertension during preeclampsia

British journal of pharmacology, 2019-06, Vol.176 (12), p.1914-1921

2019

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Role of Mitochondrial Dysfunction and Reactive Oxygen Species in Mediating Hypertension in the Reduced Uterine Perfusion Pressure Rat Model of Preeclampsia

Hypertension (Dallas, Tex. 1979), 2018-09, Vol.72 (3), p.703-711

2018

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Natural killer cells mediate pathophysiology in response to reduced uterine perfusion pressure

Clinical science (1979), 2017-12, Vol.131 (23), p.2753

2017

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Circulating Total Cell-Free DNA Levels Are Increased in Hypertensive Disorders of Pregnancy and Associated with Prohypertensive Factors and Adverse Clinical Outcomes

International journal of molecular sciences, 2021-01, Vol.22 (2), p.564

2021

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Serelaxin improves the pathophysiology of placental ischemia in the reduced uterine perfusion pressure rat model of preeclampsia

American journal of physiology. Regulatory, integrative and comparative physiology, 2016-12, Vol.311 (6), p.R1158-R1163

2016

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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, 2024-02, Vol.13 (4), p.e031417-e031417

2024

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Tumor necrosis factor alpha (TNF-α) blockade improves natural killer cell (NK) activation, hypertension, and mitochondrial oxidative stress in a preclinical rat model of preeclampsia

Hypertension in pregnancy, 2020-10, Vol.39 (4), p.399-404

2020

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Increased NOS coupling by the metabolite tetrahydrobiopterin (BH4) reduces preeclampsia/IUGR consequences

Redox biology, 2022-09, Vol.55, p.102406, Article 102406

2022

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Effects of NAMPT polymorphisms and haplotypes on circulating visfatin/NAMPT levels in hypertensive disorders of pregnancy

Hypertension research, 2015-05, Vol.38 (5), p.361-366

2015

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The role of immune cells and mediators in preeclampsia

Nature reviews. Nephrology, 2023-04, Vol.19 (4), p.257

2023

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Characterization of Mitochondrial Bioenergetics in Preeclampsia

Journal of clinical medicine, 2021-10, Vol.10 (21), p.5063

2021

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Low Dose of IL-2 Normalizes Hypertension and Mitochondrial Function in the RUPP Rat Model of Placental Ischemia

Cells (Basel, Switzerland), 2021-10, Vol.10 (10), p.2797

2021

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Investigation of interleukin-2-mediated changes in blood pressure, fetal growth restriction, and innate immune activation in normal pregnant rats and in a preclinical rat model of preeclampsia

Biology of sex differences, 2021-01, Vol.12 (1), p.4-10, Article 4

2021

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Progesterone Induced Blocking Factor Reduces Hypertension and Placental Mitochondrial Dysfunction in Response to sFlt-1 during Pregnancy

Cells (Basel, Switzerland), 2021-10, Vol.10 (11), p.2817

2021

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Progesterone supplementation attenuates hypertension and the autoantibody to the angiotensin II type I receptor in response to elevated interleukin-6 during pregnancy

American journal of obstetrics and gynecology, 2014-08, Vol.211 (2), p.158.e1-158.e6

2014

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Placental CD4+ T cells from preeclamptic patients cause autoantibodies to the angiotensin II type I receptor and hypertension in a pregnant rat model of preeclampsia

Exploration of medicine, 2022, Vol.3 (1), p.99-111

2022

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Preeclampsia: long-term consequences for vascular health

Vascular health and risk management, 2015-01, Vol.11 (default), p.403-415

2015

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Identifying immune mechanisms mediating the hypertension during preeclampsia

American journal of physiology. Regulatory, integrative and comparative physiology, 2016-07, Vol.311 (1), p.R1-R9

2016

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Blockade of endogenous angiotensin II type I receptor agonistic autoantibody activity improves mitochondrial reactive oxygen species and hypertension in a rat model of preeclampsia

American journal of physiology. Regulatory, integrative and comparative physiology, 2020-02, Vol.318 (2), p.R256-R262

2020

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Reduced uterine perfusion pressure T-helper 17 cells cause pathophysiology associated with preeclampsia during pregnancy

American journal of physiology. Regulatory, integrative and comparative physiology, 2016-12, Vol.311 (6), p.R1192-R1199

2016

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CD4+T Cells cause increased glucose, mitochondrial dysfunction, and hypertension in a Novel Pregnant Rodent Model of Gestational Diabetes Mellitus

The FASEB journal, 2022-05, Vol.36 (S1), p.n/a

2022

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An increased population of regulatory T cells improves the pathophysiology of placental ischemia in a rat model of preeclampsia

American journal of physiology. Regulatory, integrative and comparative physiology, 2015-10, Vol.309 (8), p.R884-R891

2015

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17-Hydroxyprogesterone Caproate Significantly Improves Clinical Characteristics of Preeclampsia in the Reduced Uterine Perfusion Pressure Rat Model

Hypertension (Dallas, Tex. 1979), 2015-01, Vol.65 (1), p.225-231

2015

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The role of inflammation in the pathology of preeclampsia

Pathophysiology and Current Clinical Management of Preeclampsia

Inflammatory mediators: a causal link to hypertension during preeclampsia

Role of Mitochondrial Dysfunction and Reactive Oxygen Species in Mediating Hypertension in the Reduced Uterine Perfusion Pressure Rat Model of Preeclampsia

Natural killer cells mediate pathophysiology in response to reduced uterine perfusion pressure

Circulating Total Cell-Free DNA Levels Are Increased in Hypertensive Disorders of Pregnancy and Associated with Prohypertensive Factors and Adverse Clinical Outcomes

Serelaxin improves the pathophysiology of placental ischemia in the reduced uterine perfusion pressure rat model of preeclampsia

AT1-AA Is Produced in Offspring in Response to Placental Ischemia and Is Lowered by B-Cell Depletion Without Compromising Overall Offspring Health

Tumor necrosis factor alpha (TNF-α) blockade improves natural killer cell (NK) activation, hypertension, and mitochondrial oxidative stress in a preclinical rat model of preeclampsia

Increased NOS coupling by the metabolite tetrahydrobiopterin (BH4) reduces preeclampsia/IUGR consequences

Effects of NAMPT polymorphisms and haplotypes on circulating visfatin/NAMPT levels in hypertensive disorders of pregnancy

The role of immune cells and mediators in preeclampsia

Characterization of Mitochondrial Bioenergetics in Preeclampsia

Low Dose of IL-2 Normalizes Hypertension and Mitochondrial Function in the RUPP Rat Model of Placental Ischemia

Investigation of interleukin-2-mediated changes in blood pressure, fetal growth restriction, and innate immune activation in normal pregnant rats and in a preclinical rat model of preeclampsia

Progesterone Induced Blocking Factor Reduces Hypertension and Placental Mitochondrial Dysfunction in Response to sFlt-1 during Pregnancy

Progesterone supplementation attenuates hypertension and the autoantibody to the angiotensin II type I receptor in response to elevated interleukin-6 during pregnancy

Placental CD4+ T cells from preeclamptic patients cause autoantibodies to the angiotensin II type I receptor and hypertension in a pregnant rat model of preeclampsia

Preeclampsia: long-term consequences for vascular health

Identifying immune mechanisms mediating the hypertension during preeclampsia

Blockade of endogenous angiotensin II type I receptor agonistic autoantibody activity improves mitochondrial reactive oxygen species and hypertension in a rat model of preeclampsia

Reduced uterine perfusion pressure T-helper 17 cells cause pathophysiology associated with preeclampsia during pregnancy

CD4+T Cells cause increased glucose, mitochondrial dysfunction, and hypertension in a Novel Pregnant Rodent Model of Gestational Diabetes Mellitus

An increased population of regulatory T cells improves the pathophysiology of placental ischemia in a rat model of preeclampsia

17-Hydroxyprogesterone Caproate Significantly Improves Clinical Characteristics of Preeclampsia in the Reduced Uterine Perfusion Pressure Rat Model

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