| Autor: |
Opichka MA; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA., Rappelt MW; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA., Gutterman DD; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA., Grobe JL; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Neuroscience Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Comprehensive Rodent Metabolic Phenotyping Core, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Department of Biomedical Engineering, Medical College of Wisconsin, Milwaukee, WI 53226, USA., McIntosh JJ; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.; Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. |
| Abstrakt: |
Preeclampsia is a life-threatening pregnancy-associated cardiovascular disorder characterized by hypertension and proteinuria at 20 weeks of gestation. Though its exact underlying cause is not precisely defined and likely heterogenous, a plethora of research indicates that in some women with preeclampsia, both maternal and placental vascular dysfunction plays a role in the pathogenesis and can persist into the postpartum period. Potential abnormalities include impaired placentation, incomplete spiral artery remodeling, and endothelial damage, which are further propagated by immune factors, mitochondrial stress, and an imbalance of pro- and antiangiogenic substances. While the field has progressed, current gaps in knowledge include detailed initial molecular mechanisms and effective treatment options. Newfound evidence indicates that vasopressin is an early mediator and biomarker of the disorder, and promising future therapeutic avenues include mitigating mitochondrial dysfunction, excess oxidative stress, and the resulting inflammatory state. In this review, we provide a detailed overview of vascular defects present during preeclampsia and connect well-established notions to newer discoveries at the molecular, cellular, and whole-organism levels. |
